This Week in HIV Research: Food, It Does a Body Good

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Thanks for joining us for another week recapping notable incremental findings in the world of clinically relevant HIV research. This week, we learn more about:

  • The inflammation risks heightened by unreliable access to nutritious food.
  • The wide racial disparity in the prevalence of human papillomavirus type 16, a leading cause of cervical cancer.
  • The effect of antiretroviral therapy initiation on pre-existing neurocognitive impairment.
  • The uncertain impact of low-level central nervous system inflammation in people who have been on successful HIV treatment for many years.

Come along as we explore each of these studies in a bit more detail. To beat HIV, you have to follow the science!

Barbara Jungwirth is a freelance writer and translator based in New York. Follow Barbara on Twitter: @reliabletran.

Myles Helfand is the executive editor and general manager of TheBody and TheBodyPRO. Follow Myles on Twitter: @MylesatTheBody.


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Food Insecurity Increases Inflammation Markers in Women With HIV

Women living with HIV (WLHIV) who could not count on a steady supply of nutritious food had higher levels of inflammatory markers than did WLHIV without such worries, a study published in Journal of Infectious Diseases showed.

Seventy-nine percent of 421 participants were virally suppressed. The 31% of participants who were food insecure showed 1.23 times higher levels of pro-inflammatory cytokine IL-6 and 1.13 times higher levels of tumor necrosis factor 1. The finding held independent of viral suppression or nutritional factors. Thus, lower treatment adherence or higher levels of diabetes and/or obesity are unlikely to explain these results, study authors noted.

The researchers pointed to greater stress, lower tryptophan levels, and the effect of diet on gut microbiota as other possible factors, and called for further studies into all of these issues. "These findings reinforce the need for HIV care and treatment services to incorporate programming that addresses food insecurity," they concluded.


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HPV16 Prevalence Differs by Race Among Women With HIV and Cervical Precancer

Among women living with HIV who have cervical precancer, human papillomavirus (HPV) type 16 is significantly less prevalent among women of color living with HIV than white women living with HIV, a study published in AIDS found. Worldwide, HPV types 16 and 18 cause 70% of cervical cancers and precancerous lesions.

Researchers determined the HPV types present in cervicovaginal samples of 175 women with cervical intraepithelial neoplasia stage 3 or worse. Among the 154 study participants living with HIV, 62% of white women had HPV16, while 27% of African-American women and 37% of Latinas did. After controlling for several factors in multivariate logistic regression models (notably including CD4 count), the reduced risk of HPV16 only remained for African-American women, not Latinas.

The bivalent HPV vaccine targets HPV16 and HPV18, and has been shown to have greater immunogenicity than other such vaccines, which may be important in people with impaired immune systems. However, a broader-spectrum vaccine may better cover other HPV types that cause cervical cancer among African-American WLHIV, study authors noted. They called for further research in a larger racially diverse population to determine the best approach to HPV vaccination and screening in all women living with HIV.


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Impact of HIV Treatment on Neurocognitive Impairment Varies by Baseline Symptoms

In resource-limited settings, moderate to severe neurocognitive impairment was significantly reduced in people living with HIV (PLWH) once antiretroviral therapy began, but this was not true for mild impairment, a study published in Clinical Infectious Diseases showed.

Researchers compared data on neurocognitive functioning from a clinical trial among 860 PLWH and another trial among 2,400 HIV-negative people at high risk of seroconversion. Compared to the HIV-negative cohort, 45% of PLWH had some neurocognitive impairment at (antiretroviral-naive) baseline, with 25% showing mild, 17% moderate, and 3% severe problems.

The study results included findings through 216 weeks of follow-up, but impairment rating data was only assessed between weeks 48 and 168 to mitigate potential confounders, such as practice/learning effects. At the last study visit, a third of impaired participants had improved their neurocognitive functioning. The results did not differ by antiretroviral regimen.

In those with mild symptoms at baseline, lower rates of improvement may be due to neuronal injury prior to starting treatment or ongoing inflammation despite viral suppression, study authors hypothesized. The latter issue might be addressed by adding anti-inflammatory agents to treatment regimens, they suggested.


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Study Explores Low-Level Immune Activation in the Brains of Long-Term Virally Suppressed People

While more than half of long-term virally suppressed participants in a small study published in AIDS showed markers of low-grade immune activation in the central nervous system (CNS), such markers were not associated with lower neurocognitive performance and were "likely clinically benign in most cases," according to the study authors.

Researchers studied blood and cerebrospinal fluid (CSF) samples from 20 people living with HIV whose virus had been suppressed for a median of 13.2 years. None of the participants showed neurocognitive impairment at baseline. In follow-up surveys, no participant reported any change in everyday function due to cognitive impairment. That said, 14 of the 20 participants completed a neurocognitive evaluation, and data indicated a slightly lower mean performance relative to what would be expected of similarly aged people.

One of the immune activation markers, CSF neopterin, decreased with antiretroviral therapy, but remained above the normal range in 55% of participants. The other, neurofilament light protein, dropped to within the normal range for participants' ages while on treatment.

While no participant experienced treatment failure, antiretroviral regimens did change as newer medications became available. Use of these newer drugs, as well as earlier treatment initiation, may impact CNS immune activation over time, study authors noted. They called for further studies on this question, as well as on the interplay of aging-related cognitive function and HIV-related immune activation.