3 Surprising Ways That STDs Increase HIV Risk

How the Body's Immune System Can Unwittingly Facilitate HIV Infection

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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.

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 90% 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 200% 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 (as measured by the CD4 count).

This highlights the greater need for syphilis surveillance in high-risk populations, particularly men who have sex with men (MSM) who account for 83% of syphilis cases in men and 30% 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.

Sources:

U.S. Centers for Disease Control and Prevention (CDC). "Sexually Transmitted Diseases - Reported Cases and Rates of Reported Cases per 100,000 Population, United States, 1941-2014." Atlanta, Georgia; page updated November 17, 2015; accessed January 5, 2016.

Johnson, L. and Lewis, D. "The effect of genital tract infections on HIV-1 shedding in the genital tract: a systematic review and meta-analysis." Sexually Transmitted Diseases. November 2008; 35(11):946-959.

Chun, H.; Carpenter, R.; Macalino, G.; et al. "The Role of Sexually Transmitted Infections in HIV-1 Progression: A Comprehensive Review of the Literature." Journal of Sexually Transmitted Diseases. May 28, 2012; Vol 2013; article ID 176459:1-15.

Jarzebowski, W.; Caumes, E.; Dupin, N.; et al. "Effect of early syphilis infection on plasma viral load and CD4 cell count in human immunodeficiency virus-infected men: results from the FHDH-ANRS CO4 cohort." Archives of Internal Medicine. September 10, 2012; 172(16):1237-1243.

CDC. "Reported Cases of Sexually Transmitted Diseases on the Rise, Some at Alarming Rate." NCHHSTP Newsroom. Atlanta, Georgia; press release issued November 17, 2015.

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