Most strikingly perhaps, the number of chlamydia cases has nearly doubled in the course of a single decade, rising from. While it is well known that STDs can significantly increase a person’s risk of getting HIV, many people still don’t fully understand why this is or the ways in which STDs can readily facilitate infection—even in otherwise low-risk activities like oral sex. The fact that many of these diseases remain undiagnosed only adds to the odds of getting infected. While it is clear that ulcerative infections like syphilis—which can manifest with open sores on the genitals—provide an easy route of access for the virus, around of cases have no sores. Moreover, syphilitic ulcers in the rectum or cervix are often entirely missed or unnoticed, creating a window of increased vulnerability for the duration of the primary infection (approximately weeks).
But does this mean that ulcerative infections like syphilis are somehow “worse” than other STDs when it comes to HIV? Let us look at three reasons why this may not be the case. Whenever a pathogen (i.e., a disease-causing agent) enters the body, the immune system will immediately activate, resulting in a natural, inflammatory response. Inflammation pep hiv occurs simply because the immune function is kicked into high gear, generating a plethora of immune cells to isolate and kill the pathogen. In a localized infection, such as an STD, defensive cells such as CD and CD T-cells are recruited to the front lines. CD T-cells are “helper” cells that essentially direct the “killer” CD T-cells to neutralize the pathogen. The irony is that the very cells meant to signal the attack—the CD4 cells—are the ones preferentially targeted by HIV for infection. Therefore, the more robust the pathogenic attack, the more target cells are recruited and the more likely that HIV will be able to penetrate the body’s primary immune defenses.
It is why even bacterial activity beneath the foreskin of the penis can increase the potential for HIV acquisition since the accumulation of bacterium can readily spark an immune response. So even if an STD doesn’t visibly compromise tissues of the genitals, rectum or throat, the high concentration of immune cells at the site of infection provides HIV a greater opportunity to thrive, particularly if the infection is left untreated. In the same way that an STD can increase a person’s vulnerability to HIV, an STD can also increase a person’s risk of passing the virus to others. Inflammation is, again, the primary cause, wherein immune cells are aggressively recruited to the site of the localized infection. When this happens, a process called “HIV shedding” can occur. This is defined as the sudden reactivation of dormant HIV, which up until this has been resting in hidden cellular reservoirs. As a result of this shedding, the newly activated HIV can multiply and infiltrate vaginal fluids and semen, increasing in numbers far beyond what would occur without an STD. According to a 2008 meta-analysis from the University of Cape Town’s School of Public Health and Family Medicine, HIV shedding in the genital tract is nearly doubled as a result of an active gonorrheal or chlamydial infection. Worse yet, it can do so whether a person is being treated for HIV or not. Research has shown that, in the presence of a sexually transmitted infection, a person on HIV therapy can have detectable virus in genital secretions even if the viral load in their blood is fully suppressed.
Some STDs Can Cause HIV to “Rebound”
One of the primary goals of antiretroviral therapy (ART) is to fully suppress HIV to undetectable levels. In doing so, the person with HIV is far less likely to infect others. In fact, most research seems to indicate that an HIV-infected person is more than less likely to infect a committed, non-HIV-infected partner if on fully suppressive ART. However, if that person were to experience viral rebound (i.e., the sudden return of HIV activity), the risk of transmission could increase exponentially. According to researchers with France’s ANRS (National Agency for AIDS and Hepatitis Research), persons with HIV have a nearly greater risk of viral rebound if co-infected with syphilis. On average, primary syphilis infection results in at least a five-fold viral load increase in HIV-infected men. This includes men on continuous, fully suppressive ART, and occurs irrespective of age, sexual orientation, or immune status (count). This highlights the greater need for syphilis surveillance in high-risk populations, particularly men who have sex with men (MSM) who account for of syphilis cases in men and of all new HIV diagnoses in the U.S. While there doesn’t appear to be any association between other STDs and the risk of viral rebound, the on-going risk of transmission remains high in persons untreated for HIV. In an attempt to explore the temporal relationship between STI and HIV, Zetola and colleagues used different study designs to analyse the same population. They studied 36 cases of acute HIV infection in men who have sex with men (MSM), and used a variety of control groups, including one cross over design in which participants acted as their own controls, to better describe time-dependent risk factors and control for confounding. They found that having had an STI in the previous three months was more strongly associated with HIV acquisition that having had STI months before.