The rate of sexually transmitted diseases (STDs) in the U.S. is on the rise. From 2013 to 2014 alone, the number of syphilis cases jumped from 56,482 to 63,450, while gonorrheal infections have steadily increased, year-on-year, since 2009. Most strikingly, the number of chlamydia cases has nearly doubled in the course of a decade, rising from 929,462 in 2004 to 1,441,789 in 2014.
While it is well known that STDs can significantly increase the risk of acquiring HIV, many people still don’t fully understand why this is or the ways in which STDs can readily facilitate HIV infection—even in otherwise “low-risk” activities like oral sex. The fact that many of these diseases remain undiagnosed only adds to a person’s 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 20% 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 (3-6 weeks).
But does this mean that ulcerative infections like syphilis are somehow “worse” than other STDs insofar as HIV is concerned? Let’s look at three reasons why this may not necessarily be the case:
An STD Actively “Recruits” Cells for HIV to Infect
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 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 CD4 and CD8 T-cells are recruited to the front lines. CD4 T-cells are “helper” cells that essentially direct the “killer” CD8 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.
An STD Increases the Concentration of HIV in Genital Fluids
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.
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