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Starting antiretroviral therapy (ART) right after diagnosis does not prevent the depletion of CD4+ T cells from the gut or help restore them—and researchers at the National Institutes of Health (NIH) may have found the reason. For the first time, the NIH says, scientists have shown a relationship between high levels of a “gut-homing” protein called α4β7 and HIV health outcomes.
The researchers found that women who had more CD4+ T cells with high levels of α4β7 were more likely to become infected with HIV, and the virus damaged their immune systems more rapidly than it did in women with fewer such cells.
Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases (NIAID) and coauthor of the study paper found that HIV “preferentially infects” those cells. That leads to more HIV-infected CD4+ T cells moving to the gut, which in turn leads to extensive damage to gut-based immune cells.
In the study, which compared blood samples from 59 women shortly before they acquired HIV to those of 106 women who remained HIV negative, the risk of HIV acquisition rose by 18% for each 1% increase in α4β7 protein.
The α4β7 cells also “strongly affected” how quickly HIV damaged the immune system. CD4+ T-cell levels dropped twice as fast among women with higher pre-infection levels of α4β7. Within a few months, those women also had more HIV in the blood. The researchers say the mechanism for immune system damage was likely HIV-related damage to the gut, because higher pre-infection levels of α4β7 were associated with higher levels of a biologic marker of gut damage.
The study findings suggest that ART alone may not be enough; people with HIV may also benefit from interventions to restore CD4+ T cells in their gastrointestinal tracts. One possible solution could be vedolizumab, an anti- α4β7 antibody approved for treatment of ulcerative colitis and Crohn disease. In animal studies, vedolizumab contributed to “near replenishment” of CD4+ T cells.
To determine whether short-term treatment with vedolizumab in combination with ART could generate sustained HIV remission, NIAID has initiated an early-phase clinical trial.
Source:
US Department of Health and Human Services. National Institutes of Health. https://www.nih.gov/news-events/news-releases/study-links-gut-homing-protein-levels-hiv-infection-risk-disease-progression. Published January 24, 2018. Accessed April 19, 2018.
Starting antiretroviral therapy (ART) right after diagnosis does not prevent the depletion of CD4+ T cells from the gut or help restore them—and researchers at the National Institutes of Health (NIH) may have found the reason. For the first time, the NIH says, scientists have shown a relationship between high levels of a “gut-homing” protein called α4β7 and HIV health outcomes.
The researchers found that women who had more CD4+ T cells with high levels of α4β7 were more likely to become infected with HIV, and the virus damaged their immune systems more rapidly than it did in women with fewer such cells.
Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases (NIAID) and coauthor of the study paper found that HIV “preferentially infects” those cells. That leads to more HIV-infected CD4+ T cells moving to the gut, which in turn leads to extensive damage to gut-based immune cells.
In the study, which compared blood samples from 59 women shortly before they acquired HIV to those of 106 women who remained HIV negative, the risk of HIV acquisition rose by 18% for each 1% increase in α4β7 protein.
The α4β7 cells also “strongly affected” how quickly HIV damaged the immune system. CD4+ T-cell levels dropped twice as fast among women with higher pre-infection levels of α4β7. Within a few months, those women also had more HIV in the blood. The researchers say the mechanism for immune system damage was likely HIV-related damage to the gut, because higher pre-infection levels of α4β7 were associated with higher levels of a biologic marker of gut damage.
The study findings suggest that ART alone may not be enough; people with HIV may also benefit from interventions to restore CD4+ T cells in their gastrointestinal tracts. One possible solution could be vedolizumab, an anti- α4β7 antibody approved for treatment of ulcerative colitis and Crohn disease. In animal studies, vedolizumab contributed to “near replenishment” of CD4+ T cells.
To determine whether short-term treatment with vedolizumab in combination with ART could generate sustained HIV remission, NIAID has initiated an early-phase clinical trial.
Source:
US Department of Health and Human Services. National Institutes of Health. https://www.nih.gov/news-events/news-releases/study-links-gut-homing-protein-levels-hiv-infection-risk-disease-progression. Published January 24, 2018. Accessed April 19, 2018.
Starting antiretroviral therapy (ART) right after diagnosis does not prevent the depletion of CD4+ T cells from the gut or help restore them—and researchers at the National Institutes of Health (NIH) may have found the reason. For the first time, the NIH says, scientists have shown a relationship between high levels of a “gut-homing” protein called α4β7 and HIV health outcomes.
The researchers found that women who had more CD4+ T cells with high levels of α4β7 were more likely to become infected with HIV, and the virus damaged their immune systems more rapidly than it did in women with fewer such cells.
Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases (NIAID) and coauthor of the study paper found that HIV “preferentially infects” those cells. That leads to more HIV-infected CD4+ T cells moving to the gut, which in turn leads to extensive damage to gut-based immune cells.
In the study, which compared blood samples from 59 women shortly before they acquired HIV to those of 106 women who remained HIV negative, the risk of HIV acquisition rose by 18% for each 1% increase in α4β7 protein.
The α4β7 cells also “strongly affected” how quickly HIV damaged the immune system. CD4+ T-cell levels dropped twice as fast among women with higher pre-infection levels of α4β7. Within a few months, those women also had more HIV in the blood. The researchers say the mechanism for immune system damage was likely HIV-related damage to the gut, because higher pre-infection levels of α4β7 were associated with higher levels of a biologic marker of gut damage.
The study findings suggest that ART alone may not be enough; people with HIV may also benefit from interventions to restore CD4+ T cells in their gastrointestinal tracts. One possible solution could be vedolizumab, an anti- α4β7 antibody approved for treatment of ulcerative colitis and Crohn disease. In animal studies, vedolizumab contributed to “near replenishment” of CD4+ T cells.
To determine whether short-term treatment with vedolizumab in combination with ART could generate sustained HIV remission, NIAID has initiated an early-phase clinical trial.
Source:
US Department of Health and Human Services. National Institutes of Health. https://www.nih.gov/news-events/news-releases/study-links-gut-homing-protein-levels-hiv-infection-risk-disease-progression. Published January 24, 2018. Accessed April 19, 2018.