HealthDay News — Cholesterol metabolism may be associated with a lack of HIV-1 trans infection, seen in HIV-1 infected nonprogressors (NPs), according to researchers.
Noting that HIV-1 infected NPs inhibit disease progression without antiretroviral therapy, Giovanna Rappocciolo, PhD, of the University of Pittsburgh, and colleagues examined mechanisms for this resistance to disease progression. Their findings were published in mBio.
The two types of professional antigen presenting cells (APCs) (dendritic cells and B lymphocytes) from NPs were unable to mediate HIV-1 trans infection of CD4+ T cells, while HIV-1 transinfection was effectively mediated by APCs from HIV-1 infected progressors (PRs) and HIV-1 seronegatives (SNs). Similarly efficient direct cis infection of T cells with HIV-1 was seen among NPs, PRs, and SNs.
There was a link between a lack of HIV-1 trans infection in NPs with lower cholesterol levels; and in APCs, but not T cells, there was an increase in the levels of the ATP-binding cassette, reverse cholesterol transporter ABCA1 in NPs. Reconstitution of cholesterol and inhibiting ABCA1 by messenger RNA interference restored transinfection mediated by APCs from NPs.
“The present study supports these relationships among cholesterol levels, ABCA1 activity, and HIV-1 infectivity with the demonstration that altered lipid metabolism in professional APC, i.e., DC and B lymphocytes, results in a remarkable control of HIV-1 trans infection related to a lack of HIV-1 disease progression,” wrote the researchers.
“This finding could be of importance in devising strategies for enhancing the control of HIV-1 infection.”