I am JaKePositive...I am a Homosexual...I am a Filipino...I am a Proud Ilonggo... I am HIV + since June 2010... I started my ARV Treatment May 4,2013 since my CD4 dropped to 107... I am here to RAISE AWARENESS... I am here to ENCOURAGE HIV TESTING... I am here to SUPPORT MY BROTHER'S and SISTER'S who are living with HIV... I am an ADVOCATE FOR CHANGE...

Wednesday, October 17, 2012

Human Papillomavirus (HPV) and MEN


What is a Human Papillomavirus (HPV)?

Genital human papillomavirus (HPV) is a common virus. Most sexually active people in the will have HPV at some time in their lives. There are more than 40 types of HPV that are passed on through sexual contact. These types can infect the genital areas of men, including the skin on and around the penis or anus. They can also infect the mouth and throat.

  • Genital warts usually appear as a small bump or groups of bumps in the genital area. They can be small or large, raised or flat, or shaped like a cauliflower. Health care providers can diagnose warts by looking at the genital area during an office visit. Warts can appear within weeks or months after sexual contact with an infected partner—even if the infected partner has no signs of genital warts. If left untreated, genital warts might go away, remain unchanged, or increase in size or number. Warts will not turn into cancer.
  • Anal warts (also called "condyloma acuminata") are a condition that affects the area around and inside the anus. They may also affect the skin of the genital area. They first appear as tiny spots or growths, perhaps as small as the head of a pin, and may grow larger than the size of a pea. Usually, they do not cause pain or discomfort to afflicted individuals. As a result, patients may be unaware that the warts are present. Some patients will experience symptoms such as itching, bleeding, mucus discharge and/or a feeling of a lump or mass in the anal area.

How do Men get HPV?

HPV is passed on through genital contact—most often during vaginal and anal sex. HPV may also be passed on during oral sex. Since HPV usually causes no symptoms, most men and women can get HPV—and pass it on—without realizing it. People can have HPV even if years have passed since they had sex. Even men with only one lifetime sex partner can get HPV.

What are the health problems caused by HPV in men?

Most men who get HPV (of any type) never develop any symptoms or health problems. But some types of HPV can cause genital warts. Other types can cause cancers of the penis, anus, or oropharynx (back of the throat, including base of the tongue and tonsils.) The types of HPV that can cause genital warts are not the same as the types that can cause cancer.

Note: Anal cancer is not the same as colorectal cancer. Colorectal cancer is more common than anal cancer, and is not caused by HPV.

How common are HPV-related health problems in men?

About 1% of sexually active men in the U.S. have genital warts at any one time.

Cancers of the penis, anus and oropharynx are uncommon, and only a subset of these cancers are actually related to HPV. Each year in the U.S. there are about:
400 men who get HPV-related cancer of the penis
1,500 men who get HPV-related cancer of the anus
5,600 men who get cancers of the oropharynx (back of throat), but many of these cancers are related to tobacco and alcohol use, not HPV.

Some men are more likely to develop HPV-related diseases than others:

Gay and bisexual men (who have sex with other men) are about 17 times more likely to develop anal cancer than men who only have sex with women.

Men with weakened immune systems, including those who have HIV, are more likely than other men to develop anal cancer. Men with HIV are also more likely to get severe cases of genital warts that are harder to treat.

What are the signs and symptoms?

Most men who get HPV never develop any symptoms or health problems. But for those who do develop health problems, these are some of the signs and symptoms:

One or more growths on the penis, testicles, groin, thighs, or in/around the anus.
Warts may be single, grouped, raised, flat, or cauliflower-shaped. They usually do not hurt.
Warts may appear within weeks or months after sexual contact with an infected person.

Is there a test for HPV in men?

Currently, there is no HPV test recommended for men. The only approved HPV tests on the market are for screening women for cervical cancer. They are not useful for screening for HPV-related cancers or genital warts in men.

There is no approved test to find genital warts for men or women. However, most of the time, you can see genital warts. If you think you may have genital warts, you should see a health care provider.

There is no test for men to check one’s overall “HPV status.” But HPV usually goes away on its own, without causing health problems. So an HPV infection that is found today will most likely not be there a year or two from now. 

You can check for any abnormalities on your penis, scrotum, or around the anus. See your doctor if you find warts, blisters, sores, ulcers, white patches, or other abnormal areas on your penis—even if they do not hurt.

Is there a treatment or cure for HPV?

There is no treatment or cure for HPV. But there are ways to treat the health problems caused by HPV in men.

Genital warts can be treated with medicine, removed (surgery), or frozen off. Some of these treatments involve a visit to the doctor. Others can be done at home by the patient himself. No one treatment is better than another. But warts often come back within a few months after treatment—so several treatments may be needed. 

Treating genital warts may not necessarily lower a man’s chances of passing HPV on to his sex partner. If warts are not treated, they may go away on their own, stay the same, or grow (in size or number)


Podofilox is an antimitotic drug that destroys warts, is relatively inexpensive, easy to use, safe, and self-applied. Podofilox solution should be applied with a cotton swab, or podofilox gel with a finger, to visible genital warts twice a day for 3 days, followed by 4 days of no therapy. This cycle can be repeated, as necessary, for up to four cycles. The total wart area treated should not exceed 10 cm2, and the total volume of podofilox should be limited to 0.5 mL per day. If possible, the health-care provider should apply the initial treatment to demonstrate the proper application technique and identify which warts should be treated. Mild to moderate pain or local irritation might develop after treatment. The safety of podofilox during pregnancy has not been established.

Imiquimod is a topically active immune enhancer that stimulates production of interferon and other cytokines. Imiquimod cream should be applied once daily at bedtime, three times a week for up to 16 weeks. The treatment area should be washed with soap and water 6–10 hours after the application. Local inflammatory reactions, including redness, irritation, induration, ulceration/erosions, and vesicles, are common with the use of imiquimod, and hypopigmentation has also been described. Imiquimod might weaken condoms and vaginal diaphragms. The safety of imiquimod during pregnancy has not been established.

Sinecatechin ointment, a green-tea extract with an active product (catechins), should be applied three times daily (0.5-cm strand of ointment to each wart) using a finger to ensure coverage with a thin layer of ointment until complete clearance of warts. This product should not be continued for longer than 16 weeks. The medication should not be washed off after use. Sexual (i.e., genital, anal, or oral) contact should be avoided while the ointment is on the skin. The most common side effects of sinecatechins 15% are erythema, pruritis/burning, pain, ulceration, edema, induration, and vesicular rash. This medication may weaken condoms and diaphragms. No clinical data are available regarding the efficacy or safety of sinecatechins compared with other available anogenital wart treatment modalities. The medication is not recommended for HIV-infected persons, immunocompromised persons, or persons with clinical genital herpes because the safety and efficacy of therapy in these settings has not been established. The safety of sinecatechins during pregnancy also is unknown.

Cryotherapy destroys warts by thermal-induced cytolysis. Health-care providers must be trained on the proper use of this therapy because over- and undertreatment can result in complications or low efficacy. Pain after application of the liquid nitrogen, followed by necrosis and sometimes blistering, is common. Local anesthesia (topical or injected) might facilitate therapy if warts are present in many areas or if the area of warts is large.

Pedophyllin resin 10%–25% should be applied to each wart and allowed to air-dry before the treated area comes into contact with clothing; overapplication or failure to air dry can result in local irritation caused by spread of the compound to adjacent areas. The treatment can be repeated weekly, if necessary. To avoid the possibility of complications associated with systemic absorption and toxicity, two guidelines should be followed: 1) application should be limited to <0.5 mL of podophyllin or an area of <10 cm2 of warts per session and 2) the area to which treatment is administered should not contain any open lesions or wounds. The preparation should be thoroughly washed off 1–4 hours after application to reduce local irritation. The safety of podophyllin during pregnancy has not been established. Podophyllin resin preparations differ in the concentration of active components and contaminants. The shelf life and stability of podophyllin preparations are unknown.

Trichloroacetic acid (TCA) or Bichloroacetic acid (BCA) are caustic agents that destroy warts by chemical coagulation of proteins. Although these preparations are widely used, they have not been investigated thoroughly. TCA solutions have a low viscosity comparable with that of water and can spread rapidly if applied excessively; therefore, they can damage adjacent tissues. A small amount should be applied only to the warts and allowed to dry before the patient sits or stands, at which time a white frosting develops. If pain is intense, the acid can be neutralized with soap or sodium bicarbonate. If an excess amount of acid is applied, the treated area should be powdered with talc, sodium bicarbonate (i.e., baking soda), or liquid soap preparations to remove unreacted acid. This treatment can be repeated weekly, if necessary.

Surgical therapy has the advantage of usually eliminating warts at a single visit. However, such therapy requires substantial clinical training, additional equipment, and a longer office visit. After local anesthesia is applied, the visible genital warts can be physically destroyed by electrocautery, in which case no additional hemostasis is required. Care must be taken to control the depth of electrocautery to prevent scarring. Alternatively, the warts can be removed either by tangential excision with a pair of fine scissors or a scalpel, by laser, or by curettage. Because most warts are exophytic, this procedure can be accomplished with a resulting wound that only extends into the upper dermis. Hemostasis can be achieved with an electrocautery unit or a chemical styptic (e.g., an aluminum chloride solution). Suturing is neither required nor indicated in most cases if surgical removal is performed properly. Surgical therapy is most beneficial for patients who have a large number or area of genital warts. Both carbon dioxide laser and surgery might be useful in the management of extensive warts or intraurethral warts, particularly for those persons who have not responded to other treatments.

Because all available treatments have shortcomings, some clinics employ combination therapy (simultaneous use of two or more modalities on the same wart at the same time). Data are limited regarding the efficacy or risk of complications associated with use of such combinations.


Are there ways to lower my chances of getting HPV?

A safe and effective HPV vaccine (Gardasil) can protect boys and men against the HPV types that cause most genital warts and anal cancers. It is given in three shots over six months.

Condoms (if used with every sex act, from start to finish) may lower your chances of passing HPV to a partner or developing HPV-related diseases. But HPV can infect areas that are not covered by a condom—so condoms may not fully protect against HPV.

Because HPV is so common and usually invisible, the only sure way to prevent it is not to have sexual contact. Even people with only one lifetime sex partner can get HPV, if their partner was infected with HPV.

I heard about a new HPV vaccine – can it help me?

If you are 26 or younger, there is an HPV vaccine that can help protect you against the types of HPV that most commonly cause problems in men. The HPV vaccine (Gardasil) works by preventing four common HPV types, two that cause most genital warts and two that cause cancers, including anal cancer. It protects against new HPV infections; it does not cure existing HPV infections or disease (like genital warts). It is most effective when given before a person’s first sexual contact (i.e., when s/he may be exposed to HPV).

CDC recommends the HPV vaccine for all boys ages 11 or 12, and for males through age 21, who have not already received all three doses. The vaccine is also recommended for gay and bisexual men (or any man who has sex with men), and men with compromised immune systems (including HIV) through age 26, if they did not get fully vaccinated when they were younger. The vaccine is safe for all men through age 26, but it is most effective when given at younger ages.

The HPV vaccine is very safe and effective, with no serious side effects. The most common side effect is soreness in the arm. Studies show that the vaccine can protect men against genital warts and anal cancers. It is likely that this vaccine also protects men from other HPV-related cancers, like cancers of the penis and oropharynx (back of throat, including base of tongue and tonsils), but there are no vaccine studies that have evaluated these outcomes.

I just found out that my partner has HPV …

What does it mean for my health?

Partners usually share HPV. If you have been with your partner for a long time, you probably have HPV already. Most sexually active adults will have HPV at some time in their lives. Although HPV is common, the health problems caused by HPV are much less common.

Condoms may lower your chances of getting HPV or developing HPV-related diseases, if used with every sex act, from start to finish. You may want to consider talking to your doctor about being vaccinated against HPV if you are 26 years or younger. But not having sex is the only sure way to avoid HPV.

If your partner has genital warts, you should avoid having sex until the warts are gone or removed. You can check for any abnormalities on your penis, such as genital warts. Also, you may want to get checked by a health care provider for genital warts and other sexually transmitted disease (STDs).

What does it mean for our relationship?

A person can have HPV for many years before it is found or causes health problems. So there is no way to know if your partner gave you HPV, or if you gave HPV to your partner. HPV should not be seen as a sign that you or your partner is having sex outside of your relationship.

I just found out I have genital warts …

What does it mean for me and my partner?

Having genital warts may be hard to cope with, but they are not a threat to your health. People with genital warts can still lead normal, healthy lives.

Because genital warts may be easily passed on to sex partners, you should inform them about having genital warts and avoid sexual activity until the warts are gone or removed. There are ways to protect your partner

You and your partner may benefit from getting screened for other STDs.

If used with every sex act, male latex condoms may lower your chances of passing genital warts. But HPV can infect areas that are not covered by a condom—so condoms may not fully protect against HPV.

It is important that sex partners discuss their health and risk for STIs. However, it is not clear if there is any health benefit to informing future sex partners about a past diagnosis of genital warts because it is not known how long a person remains contagious after warts are gone. 

Source: http://www.cdc.gov/std/hpv/stdfact-hpv-and-men.htm

JaKe Positive. BE SAFE! +)

Saturday, October 13, 2012

Friday, October 12, 2012

Thursday, October 11, 2012



     established in Central Philippine University in the 1970's to provide Family Planning, Screening for Reproductive Tract Infections (RTI), Counseling, Pap Smear, General Consultation and Other Services.

     located strategically beside the CPU Clinical Laboratory and CPU Birthing Center and fronting the public road.


"Realization of Exemplary Christian Education for Life through Health Care Services to the Unserved, Underserved, Underprivileged, and the Abused."


     DMPA Injection
     IUD Insertion
     Condom/Pills Dispensing
     Natural Family Planning


     Screening and Management

          Gram Staining for Gonorrhea, non-Gonorrheal Infection, 
                   Bacterial Vaginosis and Candidiasis. Price: 60 Pesos

         Pap Smear for Cervical Cancer. Price 200 Pesos

         They also facilitate other tests offered by the 
                Iloilo Social Hygiene Clinic FREE OF CHARGE.








KABALAKA REPRODUCTIVE HEALTH CENTER is located at Central Philippine University, Lopez Jaena St, Iloilo City

They are Open Weekdays 8am-5pm. 

For More information please call (033) 3209-5802.

Route from Jaro Plaza (Blue Circle) going to KABALAKA REPRODUCTIVE HEALTH CENTER (Red Circle)
At the far end of the Half Moon Field of Central Philippine University is the KABALAKA REPRODUCTIVE HEALTH CENTER (Red Circle)

              Ma'am Melba Sale

JaKe Positive. BE SAFE! +)

Tuesday, October 9, 2012


A lot of people have been sending me E-mails, Facebook Messages, Twitter Direct Messages, SMS and even calling me asking about Sexually Transmitted Infection and they want to get tested with the different STI's.


Here's a List of Services Provided by The ILOILO CITY SOCIAL HYGIENE CLINIC.

GRAM STAINING for Gonorrhea, non-Gonorrheal Infection, Bacterial Vaginosis and Candidiasis.

WET MOUNT for Trichomoniasis

Rapid Plasma Reagin (RPR) for Syphilis ( Screening Test )

Treponema Pallidum Particle Agglutination Assay ( TPHA Test) for Syphilis ( Confirmatory Test )

Distribution of Antibiotics for Sexually Transmitted Infection  ( FREE if Available ) 

They are also able to diagnose Genital herpes, Genital or Anal warts and Pubic Lice.

HIV Antibody Test with Voluntary Counseling and Testing (VCT)

These Services are Offered for FREE. 
They also Provide:

One on One Counseling

STI and HIV Education Lecture for Commercial Sex Workers every Wednesday 1pm-3pm

Community Outreach with their Trained Peer Educators conducting HIV 101 and STI Education

Mobile Voluntary Counseling and Testing ( VCT )

ILOILO CITY SOCIAL HYGIENE CLINIC  is located at Bonifacio Tanza, Iloilo City 

They are Open Weekdays 8am-5pm. 

For More information please call (033) 320-8151.

Route from Jaro Plaza (Blue Circle) going to Iloilo City Social Hygiene Clinic ( Red Circle)
Iloilo City Social Hygiene Clinic ( Red Circle)
Iloilo City Social Hygiene Clinic ( Red Circle)

The Clinic is in the 2nd floor


Source: Dr. Ma. Odeta Villaruel of ILOILO CITY SOCIAL HYGIENE CLINIC

JaKe Positive. BE SAFE! +)

Saturday, October 6, 2012


http://sourceoforigin.com/wp-content/uploads/2012/01/human-evolution.gifThe origin of AIDS and HIV has puzzled scientists ever since the illness first came to light in the early 1980's. For over 20 years it has been the subject of debates and the cause of countless arguments, with everything from a promiscuous flight attendant to a suspect vaccine programme being blamed. So what is the truth? Just where did AIDS come from?

The first recognised cases of AIDS occurred in the USA in the early 1980s. A number of gay men in New York and California suddenly began to develop rare opportunistic infections and cancers(Kaposi Sarcoma) that seemed stubbornly resistant to any treatment. At this time, AIDS did not yet have a name, but it quickly became obvious that all the men were suffering from a common syndrome.

The discovery of HIV, the Human Immunodeficiency Virus, was made soon after. While some were initially resistant to acknowledge the connection, there is now clear evidence to prove that HIV causes AIDS. So, in order to find the source of AIDS, it is necessary to look for the origin of HIV, and find out how, when and where HIV first began to cause disease in humans.

HIV is a lentivirus, and like all viruses of this type, it attacks the immune system. Lentiviruses are in turn part of a larger group of viruses known as retroviruses. The name 'lentivirus' literally means 'slow virus' because they take such a long time to produce any adverse effects in the body. They have been found in a number of different animals, including cats, sheep, horses and cattle. However, the most interesting lentivirus in terms of the investigation into the origins of HIV is the Simian Immunodeficiency Virus (SIV) that affects monkeys, which is believed to be at least 32,000 years old.


Sooty Mangabey (White-collared monkey)

It is now generally accepted that HIV is a descendant of a Simian Immunodeficiency Virus because certain strains of SIVs bear a very close resemblance to HIV-1 and HIV-2, the two types of HIV.
HIV-2 for example corresponds to SIVsm, a strain of the Simian Immunodeficiency Virus found in the sooty mangabey (also known as the White-collared monkey), which is indigenous to western Africa.
The more virulent, pandemic strain of HIV, namely HIV-1, was until recently more difficult to place. Until 1999, the closest counterpart that had been identified was SIVcpz, the SIV found in chimpanzees. However, this virus still had certain significant differences from HIV.



In February 1999 a group of researchers from the University of Alabama announced that they had found a type of SIVcpz that was almost identical to HIV-1. This particular strain was identified in a frozen sample taken from a captive member of the sub-group of chimpanzees known as Pan troglodytes troglodytes, which were once common in west-central Africa.
The researchers made the discovery during the course of a 10-year long study into the origins of the virus. They claimed that this sample proved that chimpanzees were the source of HIV-1, and that the virus had at some point crossed species from chimps to humans.
Their final findings were published two years later in Nature magazine . In this article, they concluded that wild chimps had been infected simultaneously with two different simian immunodeficiency viruses which had "viral sex" to form a third virus that could be passed on to other chimps and, more significantly, was capable of infecting humans and causing AIDS.
These two different viruses were traced back to a SIV that infected red-capped mangabeys and one found in greater spot-nosed monkeys. They believe that the hybridisation took place inside chimps that had become infected with both strains of SIV after they hunted and killed the two smaller species of monkey.
They also concluded that all three 'groups' of HIV-1 came from the SIV found in Pan troglodytes troglodytes, and that each group represented a separate crossover 'event' from chimps to humans.

HOW SIV in Primates became HIV in Humans 

It has been known for a long time that certain viruses can pass between species. Indeed, the very fact that chimpanzees obtained SIV from two other species of primate shows just how easily this crossover can occur. As animals ourselves, we are just as susceptible. When a viral transfer between animals and humans takes place, it is known as zoonosis.



The most commonly accepted theory is that of the 'hunter'. In this scenario, SIVcpz was transferred to humans as a result of chimps being killed and eaten or their blood getting into cuts or wounds on the hunter. Normally the hunter's body would have fought off SIV, but on a few occasions it adapted itself within its new human host and became HIV-1. The fact that there were several different early strains of HIV, each with a slightly different genetic make-up, would support this theory: every time it passed from a chimpanzee to a man, it would have developed in a slightly different way within his body, and thus produced a slightly different strain. 
An article published in The Lancet in 2004, also shows how retroviral transfer from primates to hunters is still occurring even today. In a sample of 1099 individuals in Cameroon , they discovered ten (1%) were infected with SFV (Simian Foamy Virus), an illness which, like SIV, was previously thought only to infect primates. All these infections were believed to have been acquired through the butchering and consumption of monkey and ape meat. Discoveries such as this have led to calls for an outright ban on bushmeat hunting to prevent simian viruses being passed to humans.

THE Oral Polio Vaccine (OPV) THEORY

Some other rather controversial theories have contended that HIV was transferred iatrogenically (i.e. via medical interventions). One particularly well-publicised idea is that polio vaccines played a role in the transfer.
In his book, The River, the journalist Edward Hooper suggests that HIV can be traced to the testing of an oral polio vaccine called Chat, given to about a million people in the Belgian Congo, Ruanda and Urundi in the late 1950s. To be reproduced, live polio vaccine needs to be cultivated in living tissue, and Hooper's belief is that Chat was grown in kidney cells taken from local chimps infected with SIVcmz. This, he claims, would have resulted in the contamination of the vaccine with chimp SIV, and a large number of people subsequently becoming infected with HIV-1.
Many people have contested Hooper's theories and insist that local chimps were not infected with a strain of SIVcmz that is closely linked to HIV. Furthermore, the oral administration of the vaccine would seem insufficient to cause infection in most people (SIV/HIV needs to get directly into the bloodstream to cause infection - the lining of the mouth and throat generally act as good barriers to the virus).
In February 2000 the Wistar Institute in Philadelphia (one of the original manufacturers of the Chat vaccine) announced that it had discovered in its stores a phial of polio vaccine that had been used as part of the program. The vaccine was subsequently analysed and in April 2001 it was announced that no trace had been found of either HIV or chimpanzee SIV. A second analysis confirmed that only macaque monkey kidney cells, which cannot be infected with SIV or HIV, were used to make Chat. While this is just one phial of many, it means that the OPV theory remains unproven.
The fact that the OPV theory accounts for just one of several different groups of HIV also suggests that transferral must have happened in other ways too, as does the fact that HIV seems to have existed in humans before the vaccine trials were ever carried out.



This is an extension of the original 'hunter' theory. In the 1950s, the use of disposable plastic syringes became commonplace around the world as a cheap, sterile way to administer medicines. However, to African healthcare professionals working on inoculation and other medical programmes, the huge quantities of syringes needed would have been very costly. It is therefore likely that one single syringe would have been used to inject multiple patients without any sterilization in between. This would rapidly have transferred any viral particles (within a hunter's blood for example) from one person to another, creating huge potential for the virus to mutate and replicate in each new individual it entered, even if the SIV within the original person infected had not yet converted to HIV.



The colonialism or 'Heart of Darkness' theory, is one of the more recent theories to have entered into the debate. It is again based on the basic 'hunter' premise, but more thoroughly explains how this original infection could have led to an epidemic. It was first proposed in 2000 by Jim Moore, an American specialist in primate behaviour, who published his findings in the journal AIDS Research and Human Retroviruses.
During the late 19th and early 20th century, much of Africa was ruled by colonial forces. In areas such as French Equatorial Africa and the Belgian Congo, colonial rule was particularly harsh and many Africans were forced into labor camps where sanitation was poor, food was scarce and physical demands were extreme. These factors alone would have been sufficient to create poor health in anyone, so SIV could easily have infiltrated the labor force and taken advantage of their weakened immune systems to become HIV. A stray and perhaps sick chimpanzee with SIV would have made a welcome extra source of food for the workers.
Moore also believes that many of the laborers would have been inoculated with unsterilized needles against diseases such as smallpox (to keep them alive and working), and that many of the camps actively employed prostitutes to keep the workers happy, creating numerous possibilities for onward transmission. A large number of laborers would have died before they even developed the first symptoms of AIDS, and those that did get sick would not have stood out as any different in an already disease-ridden population. Even if they had been identified, all evidence that the camps existed was destroyed to cover up the fact that a staggering 50% of the local population were wiped out there.

One final factor Moore uses to support his theory, is the fact that the labor camps were set up around the time that HIV was first believed to have passed into humans - the early part of the 20th century.



Some believe that HIV is a 'conspiracy' or that it is 'man-made'. A recent survey carried out in the US for example, identified a significant number of African Americans who believe HIV was manufactured as part of a biological warfare programme, designed to wipe out large numbers of black and homosexual people. Many say this was done under the auspices of the US federal 'Special Cancer Virus Program' (SCVP), possibly with the help of the CIA. Linked in to this theory is the belief that the virus was spread to thousands of people all over the world through the smallpox inoculation programme, or to gay men through Hepatitis B vaccine trials. While none of these theories can be definitively disproved, the evidence given to back them up is usually based upon supposition and speculation, and ignores the clear link between SIV and HIV or the fact that the virus has been identified in people as far back as 1959.


During the last few years it has become possible not only to determine whether HIV is present in a blood or plasma sample, but also to determine the particular subtype of the virus. Studying the subtype of virus of some of the earliest known instances of HIV infection can help to provide clues about the time it first appeared in humans and its subsequent evolution.
Four of the earliest known instances of HIV infection are as follows:
  1. A plasma sample taken in 1959 from an adult male living in what is now the Democratic Republic of the Congo.
  2. A lymph node sample taken in 1960 from an adult female, also from the Democratic Republic of the Congo.
  3. HIV found in tissue samples from an American teenager who died in St. Louis in 1969.
  4. HIV found in tissue samples from a Norwegian sailor who died around 1976.
A 1998 analysis of the plasma sample from 1959 suggested that HIV-1 was introduced into humans around the 1940s or the early 1950s.
In January 2000, the results of a new study suggested that the first case of HIV-1 infection occurred around 1931 in West Africa. This estimate (which had a 15 year margin of error) was based on a complex computer model of HIV's evolution.
However, a study in 2008 dated the origin of HIV to between 1884 and 1924, much earlier than previous estimates. The researchers compared the viral sequence from 1959 (the oldest known HIV-1 specimen) to the newly discovered sequence from 1960. They found a significant genetic difference between them, demonstrating diversification of HIV-1 occurred long before the AIDS pandemic was recognised.
The authors suggest a long history of the virus in Africa and call Kinshasa the “epicentre of the HIV/AIDS pandemic” in Central Africa. They propose the early spread of HIV was concurrent with the development of colonial cities, in which crowding of people increased opportunities for HIV transmission. If accurate, these findings imply that HIV existed before many scenarios (such as the OPV and conspiracy theories) suggest.

When was HIV-2 get passed to humans? 

Until recently, the origins of the HIV-2 virus had remained relatively unexplored. HIV-2 is thought to come from the SIV in Sooty Mangabeys rather than chimpanzees, but the crossover to humans is believed to have happened in a similar way (i.e. through the butchering and consumption of monkey meat). It is far rarer, significantly less infectious and progresses more slowly to AIDS than HIV-1. As a result, it infects far fewer people, and is mainly confined to a few countries in West Africa.
In May 2003, a group of Belgian researchers published a report in Proceedings of the National Academy of Science. By analysing samples of the two different subtypes of HIV-2 (A and B) taken from infected individuals and SIV samples taken from sooty mangabeys, Dr Vandamme concluded that subtype A had passed into humans around 1940 and subtype B in 1945 (plus or minus 16 years or so). Her team of researchers also discovered that the virus had originated in Guinea-Bissau and that its spread was most likely precipitated by the independence war that took place in the country between 1963 and 1974 (Guinea-Bissau is a former Portuguese colony). Her theory was backed up by the fact that the first European cases of HIV-2 were discovered among Portuguese veterans of the war, many of whom had received blood transfusions or unsterile injections following injury, or had possibly had relationships with local women.


The question of exactly where the transfer of HIV to humans took place, and where the 'epidemic' officially first developed has always been controversial. Some have suggested that it is dangerous to even try to find out, as AIDS has frequently been blamed on an innocent person or group of individuals in the past. However, scientists remain keen to find the true origin of HIV, as most agree it is important to understand the virus and its epidemiology in order to fight it. 

So did it definitely come from Africa? 


Given the evidence we have already looked at, it seems highly likely that Africa was indeed the continent where the transfer of HIV to humans first occurred (monkeys from Asia and South America have never been found to have SIVs that could cause HIV in humans). In May 2006, the same group of researchers who first identified the Pan troglodytes troglodytes strain of SIVcpz, announced that they had narrowed down the location of this particular strain to wild chimpanzees found in the forests of Southern Cameroon. By analysing 599 samples of chimp droppings (P. T. troglodytes are a highly endangered and thus protected species that cannot be killed or captured for testing), the researchers were able to obtain 34 specimens that reacted to a standard HIV DNA test, 12 of which gave results that were virtually indistinguishable from the reactions created by human HIV. The researchers therefore concluded that the chimpanzees found in this area were highly likely the origin of both the pandemic Group M of HIV-1 and of the far rarer Group N. The exact origins of Group O however remain unknown.
HIV Group N principally affects people living in South-central Cameroon, so it is not difficult to see how this outbreak started. Group M, the group that has caused the worldwide pandemic, was however first identified in Kinshasa, in the Democratic Republic of Congo. It is not entirely clear how it transferred from Cameroon to Kinshasa, but the most likely explanation is that an infected individual travelled south down the Sangha river that runs through Southern Cameroon to the River Congo and then on to Kinshasa, where the Group M epidemic probably began.
Just as we do not know exactly who spread the virus from Cameroon to Kinshasa, how the virus spread from Africa to America is also not entirely clear. However, recent evidence suggests that the virus may have arrived via the Caribbean island of Haiti.

Why is Haiti significant? 
Flag of Haiti
The AIDS epidemic in Haiti first came to light in the early 1980s, at around the same time that cases in the USA were being uncovered. Following the discovery of a number of Haitians with Kaposi's Sarcoma and other AIDS-related conditions, medical journals and books began to claim that AIDS had come from Haiti, and that Haitians were responsible for the AIDS epidemic in the United States.
These claims, which were often founded on dubious evidence, fuelled pre-existing racism in the US and many Haitians suffered severe discrimination and stigma as a result. A large number of Haitian immigrants living in the US lost their jobs and were evicted from their homes as Haitians were added to homosexuals, haemophiliacs and heroin users to make the 'Four-H Club' of groups at high risk of AIDS.
The emotionally-charged culture of blame and prejudice that surrounded HIV and AIDS in the early years meant that it soon became politically difficult to present epidemiological findings in a neutral and objective way. For many years the link between Haiti and the US epidemic was therefore dropped as a subject.

 In March 2007 however, it returned to the public eye at the Fourteenth Conference on Retroviruses and Opportunistic Infections (CROI) in Los Angeles. A group of international scientists presented data based on complex genetic analysis of 122 early samples of HIV-1, group M, subtype B (the most common strain found in the USA and in Haiti) showing that the strain had probably been brought to Haiti from Africa by a single person in around 1966; a time when many Haitians would have been returning from working in the Congo.

Genetic analysis then showed that subtype B spread slowly from person to person on the island, before being transferred to the US, again probably by a single individual, at some point between 1969 and 1972. A paper published in October 2007 by Worobey and colleagues gave a 99.7% certainty that HIV subtype B originated in Haiti before passing to the US.

It is possible that HIV had entered the US several times before subtype B took a firm hold (which would explain the infection of the St. Louis teenager in the early to mid-1960s), but it was the late 1960s / early 1970s transfer that is believed to be responsible for the widespread epidemic seen in the US today. Once the virus had established itself in the gay community, it would have spread fairly rapidly (anal intercourse carries a very high transmission risk), with transmission occurring within and between the US and Haiti, and internationally, until the original route taken by the virus was largely obscured. 

Dr Michael Worobey, lead researcher in the study, claimed that his data was not intended to place any blame on Haiti, or on Central Africans, and stressed that none of the people who first transmitted HIV would have been aware they were infected. His work still received strong protests from one Haitian delegate at the CROI conference however, demonstrating the extent to which tracing HIV’s origins remains a politically sensitive exercise. 

There are a number of factors that may have contributed to the sudden spread of HIV, most of which occurred in the latter half of the twentieth century. 



Both national and international travel undoubtedly had a major role in the initial spread of HIV. In the US, international travel by young men making the most of the gay sexual revolution of the late 70s and early 80s would certainly have played a large part in taking the virus worldwide. In Africa, the virus would probably have been spread along truck routes and between towns and cities within the continent itself. However, it is quite conceivable that some of the early outbreaks in African nations were not started by Africans infected with the 'original' virus at all, but by people visiting from overseas where the epidemic had been growing too. The process of transmission in a global pandemic is simply too complex to blame on any one group or individual. 

Much was made in the early years of the epidemic of a so-called 'Patient Zero' who was the basis of a complex "transmission scenario" compiled by Dr. William Darrow and colleagues at the Centre for Disease Control in the US. This epidemiological study showed how 'Patient O' (mistakenly identified in the press as 'Patient Zero') had given HIV to multiple partners, who then in turn transmitted it to others and rapidly spread the virus to locations all over the world. A journalist, Randy Shilts, subsequently wrote a book based on Darrow's findings, which named Patient Zero as a gay Canadian flight attendant called Gaetan Dugas. For several years, Dugas was vilified as a 'mass spreader' of HIV and the original source of the HIV epidemic among gay men. However, four years after the publication of Shilts' article, Dr. Darrow repudiated his study, admitting its methods were flawed and that Shilts' had misrepresented its conclusions.
While Gaetan Dugas was a real person who did eventually die of AIDS, the Patient Zero story was not much more than myth and scaremongering. HIV in the US was to a large degree initially spread by gay men, but this occurred on a huge scale over many years, probably a long time before Dugas even began to travel.

The Blood Industry


As blood transfusions became a routine part of medical practice, an industry to meet this increased demand for blood began to develop rapidly. In some countries such as the USA, donors were paid to give blood, a policy that often attracted those most desperate for cash; among them intravenous drug users. In the early stages of the epidemic, doctors were unaware of how easily HIV could be spread and blood donations remained unscreened. This blood was then sent worldwide, and unfortunately most people who received infected donations went on to become HIV positive themselves. 

In the late 1960's haemophiliacs also began to benefit from the blood clotting properties of a product called Factor VIII. However, to produce this coagulant, blood from hundreds of individual donors had to be pooled. This meant that a single donation of HIV+ blood could contaminate a huge batch of Factor VIII. This put thousands of haemophiliacs all over the world at risk of HIV, and many subsequently became infected with the virus.



The 1970s saw an increase in the availability of heroin following the Vietnam War and other conflicts in the Middle East, which helped stimulate a growth in intravenous drug use. As a result of sharing unsterilised needles and syringes, HIV was passed on among injecting drug users (IDUs). Due to this repeated practice many IDUs continue to be infected with HIV.

It is likely that we will never know who the first person was to be infected with HIV, or exactly how it spread from that initial person. Scientists investigating the possibilities often become very attached to their individual 'pet' theories and insist that theirs is the only true answer, but the spread of AIDS could quite conceivably have been induced by a combination of many different events. Whether through injections, travel, wars, colonial practices or genetic engineering, the realities of the 20th century have undoubtedly had a major role to play. Nevertheless, perhaps a more pressing concern for scientists today should not be how the AIDS epidemic originated, but how those it affects can be treated, how the further spread of HIV can be prevented and how the world can change to ensure a similar pandemic never occurs again.

SOURCE: http://www.avert.org/origin-aids-hiv.htm

JaKe Positive. BE SAFE! +)

Thursday, October 4, 2012


The 5th Annual Western Visayas AIDS Congress is a yearly gathering of HIV Support Groups in Western Visayas (Panay & Guimaras Islands and Negros Occidental) along with Government, Private, Non-Government Organizations and Other Individuals/Groups who support the HIV and AIDS ADVOCACY. It is led by The Department of Health-Center for Health Development Region 6 under the Regional Multi-Sectoral Partnership for STI, HIV & AIDS Prevention and Control (RMPSHAPC). 
This year the Congress is going to be held at Kapis Mansions, Roxas City, Capiz on October 29-31, 2012, with the theme, “Working together in sustaining HIV & AIDS initiatives in Western Visayas”. This three-day live-in activity is aimed to harmonize and scale up strategies on HIV prevention, treatment, care and support through local partnerships and community mobilization to provide quality HIV/AIDS services in Western Visayas.

JaKe Positive. BE SAFE! +)

Monday, October 1, 2012



 The decision to start a patient on ARV will be based on the clinical findings and/or CD4 level determination. The benefits, toxicity, adherence issues and costs of the treatment must be a component of counseling.

Criteria for Initiation of ARV
WHO Clinical Staging
TREAT if CD4 is BELOW 200 cells/mm3
TREAT if CD4 is BELOW 200 cells/mm3
Consider TREATMENT if CD4 is BELOW 350 cells/mm3 and initiate TREATMENT before CD4 falls below 200 cells/mm3
TREAT irrespective of CD4 Count




Persistent Generalized Lymphadenopathy
Unexplained moderate weight loss (under 10% of presumed or measured body weight)
Recurrent Upper Respiratory Tract Infections (Sinusitis, Tonsillitis, Otitis Media, Pharyngitis)
Herpes Zoster
Angular Cheilitis
Recurrent Oral Ulcerations
Papular Pruritic Eruptions
Seborrheic Dermatitis
Fungal Nail Infection
Unexplained severe weight loss ( over 10% of presumed or measured body weight)
Unexplained Chronic Diarrhea for longer than one month
Unexplained Persistent Fever (intermittent or constant for longer than one month)
Persistent Oral Candidiasis
Oral Hairy Leukopakia
Pulmonary Tuberculosis (current)
Severe Bacterial Infections (e.g. Pneumonia, Empyema, Pyomyositis, Bone or Joint Infection, Meningitis, Bacteremia, Severe Pelvic Inflammatory Disease)
Acute Necrotizing Ulcerative Stomatitis, Gingivitis, Periodontitis
Unexplained Anemia (below 8g/dl), Neutropenia (below 0.5 x 109 / 1) and/or Chronic Thrombocytopenia (below 50 x 109 / 1)
HIV Wasting Syndrome
Pneumocystis Pneumonia
Recurrent Bacterial Pneumonia
Chronic Herpes Simplex infection (Orolabial, Genital or Anorectal for more than one month’s duration or visceral at any site)
Esophageal Candidiasis (or Candidiasis of Trachea, Bronchi or Lungs)
Extrapulmonary Tuberculosis
Kaposi Sarcoma
Cytomegalovirus Infection (Retinitis or Infection of other organs)
Central Venous System Toxoplasmosis
HIV Encephalopathy
Extrapulmonary Cryptococci's incliding Meningitis
Disseminated Non-Tuberculosis Mycobacterial Infection
Progressive Multifocal Leukoencephalopathy
Chronic Cryptosporidiosis
Chronic Isosporiasis
Disseminated Mycosis (Coccidiomycosis or Histoplasmosis)
Recurrent Septicemia (including Non-Typhoidal Salmonella)
Lymphoma (Cerebral or B Cell Non-Hodgkin)
Invasive Cervical Carcinoma
Atypical Disseminated Leishmaniasis
Symptomatic HIV-Associated Neuropathy or HIV-Associated Cardiomyopathy





(ZDV or AZT)

300mg Tablets
300mg every 12 hours take without regard to meals Anemia, Leukopenia,

Lactic Acidosis (rare)
Lamivudine (3TC)

150mg Tablets
150mg every 12 hours
or 300mg once daily
take without regard to meals Well tolerated
Stavudine (d4T)

30mg Tablets
30mg every 12hours irrespective of body weight take without regard to meals Pancreatitis

Lactic Acidosis

Severe Hepatomegally
with Steatosis

Rapidly Progressing Ascending Neuromuscular Weakness
Didanosine (ddI)
200mg Entric Coated Capsules

250mg Entric Coated Capsules

400mg Entric Coated Capsules
Body weight: >60kg
400mg once daily
with TDF:
250mg once daily

Body weight: <60kg
250mg once daily
with TDF:
200mg once daily
Must be taken on an empty stomach Pancreatitis

Lactic Acidosis


Tenofovir (TDF)
300mg Tablets
300mg once daily take without regard to meals Nephrotoxicity


Efavirenz (EFV)
600mg Tablets
600mg once daily Take on an empty stomach and before bedtime as severe dizziness is possible upon initiation of therapy that resolves or becomes tolerable after a few days Rash

Nevirapine (NVP)

200mg Tablets
As severe hypersensitivity may develop during initiation, trial period should be done by giving 200mg once a day x 14days together with the full dose of NRTI. If there is no sign of hypersensitivity, then give full dose at 200my every 12hours. Take without regard to meals

Not recommended to be co-administered with Rifampicin.
STOP if any of these are observed:
1. Fever or Feverish Sensation
2. Flu-like Symptoms such as muscle or body pains
3. Disseminated Macular or Maculopapular or Urticarial rashes

In case of mild skin rashes such as discreet papular or nodular rashes that are limited in number, without other signs, continue NVP and observe for any progression.

Serious hepatic events have been reported among treatment-naïve with pre-Nevirapine CD4 counts >250 cells/mm3 or in treatment-naïve male patients with pre-Nevirapine CD4 counts >400 cells/mm3


Indinavir (IDV)
400mg Capsules
800mg every 12hours to be given with Ritonavir 100mg every 12hours For RTV-boosted IDV take with or without food

Take with plenty of water to avoid Nephrolithiasis.

Not recommended to be co-administered with Rifampicin
Ritonavir (RTV)

100mg Capsules
100mg every 12hours to be given with Indinavir 800mg every 12hours or Sauinavir 1000mg every 12hours For RTV-boosted IDV take with or without food

For RTV-boosted SQV take within 2hours of a meal

Not recommended to be co-administered with Rifampicin

Lopinavir / Ritonavir (LPV/r)

Lopinavir 200mg/Ritonavir 50mg Tablets
2 tablets every 12hours Take without regard to meals

Not recommended to be co-administered with Rifampicin
Gastro Intestinal Intolerance

Nelfinavir (NFV)

250mg Tablets 625mg Tablets
1250mg every 12hours
750mg every 8hours
Take with meal or snack

Not recommended to be co-administered with Rifampicin
Gastro Intestinal Intolerance

Saquinavir (SQV)
500mg Tablets
1000mg every 12hours to be given with Ritonavir 100mg every 12hours Take within two hours of a meal

Not recommended to be co-administered with Rifampicin
Gastro Intestinal Intolerance



Lamivudine (3TC) + Stavudine (d4T)

3TC 150mg + d4T 30mg Tablets
1 Tablet every 12hours Take without regard to meals See Lamivudine and Stavudine above
Zidovudine (ZDV) + Lamivudine (3TC)

ZDV 300mg + 3TC 150mg Tablets
1 Tablet every 12hours Take without regard to meals See Zidovudine and Lamivudine above
Zidovudine (ZDV) + Lamivudine (3TC) +
Nevirapine (NVP)

ZDV 300mg + 3TC 150mg + NVP 200mg Tablets
1 Tablet every 12hours Take without regard to meals

Not recommended to be co-administered with Rifampicin
See Zidovudine, Lamivudine and Nevirapine above
Emtricitabine (FTC) + Tenofovir (TDF) + Efavirenz (EFV)

FTC 200mg + TDF 300mg + EFV 600mg Tablets
1 Tablet once daily Take on an empty stomach and before bedtime See Tenofovir and Efavirenz above.

Emtricitabine – minimal toxicity, rare cases of lactic acidosis

HIV can develop resistance to ARV’s. The success of ARV Therapy largely depends on patient’s adherence to treatment. A 95% adherence rate is required to prevent the development of drug resistance.

Complete Blood Count (CBC)
Chest X-Ray, Sputum Acid Fast Bacilli (AFB) and Sputum Culture to rule out Active Tuberculosis
Pregnancy Test for Females of Reproductive Age
Baseline Urinalysis, Fasting Blood Sugar (FBS), Liver Function Tests, Creatinine, and Lipid Profile when indicated


For Zidovudine (AZT) + Lamivudine (3TC) + Efavirenz (EFV) / Nevirapine (NVP)
Complete Blood Count (CBC) – every month for the first 3 months and every 4-6 months thereafter
SGPT, SGOT, Alkaline Phosphatase, Amylase – after 1 month, after 6 months and every 12 months thereafter
For Tenofovir (TDF) + Lamivudine (3TC) + Efavirenz (EFV) / Nevirapine (NVP)
Creatinine and Urinalysis – Annually
SGPT, SGOT, Alkaline Phosphatase, Amylase – after 1 month, after 6 months and every 12 months thereafter
For Stavudine (d4T) + Lamivudine (3TC) + Efavirenz (EFV) / Nevirapine (NVP)
Complete Blood Count (CBC) – Annually
SGPT, SGOT, Alkaline Phosphatase, Amylase – after 1 month, after 6 months and every 12 months thereafter
Total Cholesterol, Triglyceride, Low Density Lipoprotein (LDL) – after 6 months and every 12 months thereafter
For Tenofovir (TDF) + Lamivudine (3TC) + Lopinavir / Ritonavir (LPV/r)
Creatinine and Urinalysis – Annually
Total Cholesterol, Triglyceride, Low Density Lipoprotein (LDL) – after 6 months and every 12 months thereafter
Fasting Blood Sugar (FBS) – after 6 months and every 12 months thereafter
For Zidovudine (AZT) + Lamivudine (3TC) + Lopinavir / Ritonavir (LPV/r)
Complete Blood Count (CBC) – after 1 month, after 6 months and avery 12 months thereafter
Total Cholesterol, Triglyceride, Low Density Lipoprotein (LDL) – after 6 months and every 12 months thereafter
Fasting Blood Sugar (FBS) – after 6 months and every 12 months thereafter
For Stavudine (d4T) + Lamivudine (3TC) + Lopinavir / Ritonavir (LPV/r)
Complete Blood Count (CBC) – Annually
SGPT, SGOT, Alkaline Phosphatase, Amylase – after 1 month, after 6 months and every 12 months thereafter
Total Cholesterol, Triglyceride, Low Density Lipoprotein (LDL) – after 6 months and every 12 months thereafter
Fasting Blood Sugar (FBS) – after 6 months and every 12 months thereafter

Trial of therapy for at least 6 to 12 months should be given before concluding that an ARV regimen is failing. For patients with good compliance to ART, clinical response is recommended to be used together with CD4 Count and Viral Load Determination (whenever available) to detect treatment failure.

Drug Toxicity and Side Effects
ARV Drugs are associated with side effects and long term toxicities. Although life threatening side effects had been reported, many side effects can be managed symptomatically. the ARV component causing toxicity should be identified and changed if necessary. The General Principle is that single-drug substitution because of toxicity should involve drugs belonging to the same ARV class.
It is also important to ask patients of intake of other medications because ARV’s may interact with these medications.

Treatment Failure
It is very important to regularly assess patients for treatment failure, determine the reasons for these and institute appropriate management immediately. If poor compliance is the cause of treatment failure then counseling for adherence must be intensified and the current regimen continued. Determination of CD4 Count should be performed after 3 months to reassess response to treatment.
Patients who are candidates for second-line ARV’s must be managed in close coordination with the Research Institute of Tropical Medicine or San Lazaro Hospital.


 JaKe Positive. BE SAFE! +)


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