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Relax, It's Just SEX!

Community Forum Summary

March 13, 2002

Speaker: David Evans, Assistant Director of Treatment Education, GMHC. Moderated by Tracy Swan, ACRIA.

This first quarterly community forum of 2002 aimed to encourage discussion between audience members and three panelists who volunteered to discuss issues related to communication and decision-making around sex. David Evans of GMHC began the evening with a presentation on HIV transmission, sexually transmitted diseases (STDs) and the potential for HIV re-infection/superinfection. Tracy Swan from ACRIA moderated the panel discussion.

The forum began with a brief risk-taking demonstration, asking the audience to rate various activities as safe or risky. The audience was encouraged to present alternate scenarios in which these activities became less safe or less risky. The point of the activity was to demonstrate that nearly any activity could be made safer or more risky.

The discussion was followed by a brief talk by David Evans. Evans spoke regarding possible complications that may arise when people with HIV engage in unprotected sex, such as infection with a sexually transmitted disease (STD) and the possibility of re-infection with HIV. Although we know that HIV can and does recombine (see below), at the present time there is almost no information that can confirm or rule out the possibility of HIV re-infection (also called superinfection). How are people living with HIV making decisions about sexual risk-taking without having this information?

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What Is Recombination?

PCR (polymerase chain reaction) technology has made it possible to identify and group HIV's genetic information from a blood sample. Using this information, HIV has been divided into two main groups -- type "M" for major (most HIV infections across the world are part of the family of "M" viruses) and type "O" for outlier. These two groups are then divided into sub-types based on their genetic similarities. Type "M" viruses have been classified into subtypes from A through K.

The first subtypes appear to have been caused by mutations (changes) in HIV. HIV copies itself very rapidly and is not very good at making exact copies of itself. These inexact copies are called mutations. HIV's capacity to create subtypes through mutations is limited. The virus changes so quickly that HIV's genetic information can turn from language to nonsense. Because of the potential for "nonsense" mutations, HIV subtypes aren't continuing to evolve simply as a result of mutations.

HIV subtypes have been created as a result of recombination -- when two different subtypes co-infect a cell and merge their RNA into a single piece of virus (virion). It is suspected that HIV recombination happens when a person is exposed to more than one viral subtype when they become infected with HIV. Although it is not yet clear if a person who has been living with HIV can become re-infected, people who have been infected with recombinant strains of HIV have been identified.

The first evidence to support HIV recombination came from the sabeus monkey in Africa. Sabeus monkeys were infected with a form of SIV (simian, or ape, immunodeficiency virus) that was a recombinant of African green monkey SIV and sooty mangabey SIV. Since then, people who have been infected with recombinant strains of HIV have been identified.


What About Re-Infection?

Can it happen? No one is sure. However, there's a lot of speculation about the potential consequences of re-infection, including the possibility of re-infection with virus that is resistant to one or more antiretroviral drugs. We don't know the impact of re-infection with a resistant virus on a person's response to HIV treatment. How will the immune system deal with re-infection? Could re-infection create stronger or more easily transmissible viruses? Many questions remain unanswered.


Some New Information

At the Retrovirus Conference this February, a case of superinfection was reported. The person discussed was initially infected with HIV in November of 1998. He joined a clinical trial shortly after becoming infected. During a treatment interruption two years after entering the study, his viral load spiked up to 80,000. Within two weeks, the viral load dropped down to 21,000. Shortly afterwards, his viral load increased and remained between 200,000 and 400,000 until he re-started treatment.


What Happened?

Apparently, a few weeks before the second rebound in his viral load, he had been on vacation in Brazil, where he had unprotected sex with multiple partners. Because he'd been in a clinical trial, there were stored blood samples that could be used to identify his HIV subtype, both before and after the vacation. When he joined the study, he had HIV subtype AE. After his Brazilian vacation and spike in viral load, he had HIV subtype B, which is common in Brazil. No subtype B was found in his blood before his trip. He did not re-start treatment for four months after his infection with subtype B. During this period off treatment, his viral load continued to be high and his CD4 cell count dropped by 300. However, his viral load dropped and his CD4 cell count climbed after re-starting HAART.


What Does This Mean?

Although this information has important implications, more research and information are needed to help people make informed decisions about risk.


First the Basics

In order to effectively understand the nature of HIV infection, it is important to understand the nature of the virus. Evans broke down HIV transmission into three components: quality, quantity, and route.


What You Get Is What You Get/Quality or Type of Virus

HIV is a fragile virus requiring an environment of fluid and cells in order to remain alive and infectious. Outside of this environment, HIV will not survive.

In newly infected HIV patients, the rate of infection with a virus that is already resistant to one or more drugs is growing. In some areas, up to 25% of new HIV infections are with a drug-resistant virus. The consequences of this more resistant strain are obvious; there are fewer or no treatment options. Potentially, newly HIV positive patients may be able to contract some sort of "supervirus" that exhibits resistance to a wide range of drugs and therapies, although at the present time there has not been sufficient research to document this.

HIV re-infection is theoretically possible. Not much is known about this with any degree of certainty, but in vitro (in a petri dish), such re-infection has occurred. In vivo (inside the body), the HIV has shown the uncanny ability to return to the wild-type, or original, virus. If it is possible for people to become re-infected with HIV, the potential impact of such re-infection on the person's HIV disease progression and response to anti-viral medication is not known. More research is needed to answer these questions.


Undetectable Does Not Necessarily Mean Undetectable

HIV quantity: the amount of virus varies; depending on which area of the body it comes from. For example, levels of virus in the blood are not the same as in the testes, vagina, or in the anus. When patients get viral load assays performed, an "undetectable" result may not accurately indicate the amount of virus in someone's semen, vaginal fluid or in the anus -- these levels may be higher than those found in blood. "Undetectable" does not mean a person is no longer infectious, but studies in Africa have shown a reduced rate of sexual transmission of HIV when men and women with undetectable blood viral loads engage in sex with a negative partner.

However, there are other risk factors that may increase the likelihood of HIV transmission, such as sexually transmitted diseases (STDs). Levels of HIV in people with STDs are 5-7 times greater, Evans reports. Studies have been done to examine the HIV transmission rates among patients with STDs. Some studies show a reduction in HIV transmission rates while the STDs are being treated. Other studies do not show these results. However, when a person is infected with an STD, white blood cells, especially macrophages and dendritic cells gather to the site of infection. CD4 cells can cluster around any type of lesion, sore, inflammation or opening in the skin as part of the body's immune response. These immune cells can easily become infected with HIV and carry the virus to other parts of the body.


Route of Entry

Certain areas of the body are more susceptible to infection than others. Mucosa, present in the lining of the anus, mouth, and vagina, are very susceptible to HIV infection. Anal sex may lead to increased rates of transmission due to the trauma caused during sex. As a penis enters the anus, the trauma signals the CD4 cells to gather in the area of "distress." CD4 cells are called to lead the attack against the cause of the trauma. These CD4 cells are potential targets for HIV.

A current area of controversy is whether or not an uncircumcised penis is more susceptible to infection than a circumcised penis. Studies are showing that circumcised men are at a lower risk for infection than uncircumcised men, but no conclusive data have been released to date.

When discussing HIV transmission, people tend to describe sexual acts as less or more risky. The amount of HIV in a person's semen or vaginal fluid can increase or decrease the risk of HIV infection, and certain sexual acts are riskier than others. Evans engaged the audience in another interactive discussion in which a hypothetical scenario was presented involving risky behavior of an HIV positive man. In a given evening, the individual engages in sex with many partners. Although the individual described in the scenario is using condoms both as a "top" and a "bottom" during anal sex, he could still be at risk for STD infection by receiving oral sex without a condom. In addition, condoms do not offer full body protection against herpes, syphilis and HPV because there may be warts, lesions or chancres present in areas that a condom does not cover. There is also some risk of HIV infection for a partner performing oral sex, although there are several options to reduce the amount of risk involved. If there are no open cuts or sores in a person's mouth, and the partner does not ejaculate inside a person's mouth, the risk of HIV infection from oral sex is lower. However, this will not reduce the risk of STD infection from oral sex.

Three male volunteers were introduced to the audience. Two of the men were uninfected; the other was recently infected and fielded questions about how he became infected with HIV. He was frank about the circumstances surrounding his situation and told the audience he contracted the virus through unprotected sex with other men. He touched upon issues about the difficulty of discussing HIV with a sexual partner, and the audience contributed various experiences, strategies and philosophies about communication, negotiation, responsibility and impact of the nature of the relationship ("booty call" vs. boyfriend or partner).


Conclusion

The message of the evening was an overwhelming emphasis that there is always some risk in sexual activity. Whether or not you are living with HIV, it is extremely important to have access to information about potential risks and risk reduction options to help make informed decisions about sex. The absence of any hard data, and the emotional complexities surrounding sex can complicate decisions about risk taking.


  
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This article was provided by AIDS Community Research Initiative of America. Visit ACRIA's website to find out more about their activities, publications and services.
 
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