| dc.description.abstract | Background: Remaining as one of the infectious agents associated with major global health
burdens, to date, there is no effective vaccine/drug to HIV and the available anti-retroviral
therapy (ART) only prolongs the lives of the infected people. Exposure to HIV has been shown
to either lead to established infection or no infection. Why some people don’t get infected has
not been fully understood. Studies on other viruses that modulate HIV infection may shed some
light on this unique phenomenon. Human herpesvirus 7 (HHV7) is the only other virus known to
use the CD4 surface glycoprotein exclusively as its primary receptors into the CD4+ T cells. This
virus has been shown to down-regulate surface expression of these receptors in in-vitro studies
hence interfere with HIV infection into these cells.
Objectives: The study aimed at assessing the impact of HHV7 infection on expression of
CD4+ T cell surface receptors used by HIV for entry into the host cells.
Methodology: This was a cross sectional cohort study where HIV discordant couples aged
between 18 and 50 years in the Pumwani discordant couples’ cohort were recruited. A calculated
sample size of 125 study participants was used. Participants were categorized into Highly
exposed seronegative (HESN), HIV positive and HIV negative controls. Laboratory procedures
included PCR and Flow cytometry to detect and quantify HHV7 genome and the surface
expression levels of the CD4+ T cell surface receptors in the genital mucosa respectively.
Results: HHV7 was more prevalent in males and the viral loads were significantly higher in the
males regardless of their HIV status. CD4+ T cell frequencies were higher in the HHV7+
controls. This was also observed in cases that were negative for both HHV7 and HIV. There was
a strong positive correlation between HHV7 viral loads and CD4+ T cell frequencies. The
expression levels of the CD4 receptors were reduced in HHV7+ subjects. A negative correlation
was observed between HHV7 viral loads and CD4 receptor expression. CCR5 expression was
higher in both HHV7+ and HIV+ subjects. However, a negative correlation was observed
between HHV7 viral loads and CCR5 expression levels.
Conclusion: The study results support findings from previous in-vitro studies which
demonstrated HHV7 induced inhibition of HIV-1 infection into the CD4+ T cells. In addition, an
increase in the CD4+ T cell frequencies was observed in the HHV7+ control population. In
conclusion, the study proposes that HHV7 could be the agent behind the HIV infection resistance
of the HESN group in the study population | en_US |
