UCSF Logo Low level HIV viremia is a condition where the HIV levels in the bloodstream are low and therefore unidentifiable by standard blood tests. In this research, University of California scientists have stated that the prevalence of low level HIV viremia may not be a risk factor for excessive blood markers linked to inflammation and coagulation or death in patients exposed to highly active anti-retroviral therapy (HAART) for HIV.

Usually, patients on HAART are inspected regularly in a gap of 3 months to help maintain their HIV levels below the threshold diagnosable by standard trials. Initial studies have shown HAART patients who have low HIV levels could have increasing markers of inflammation and coagulation that is related to cardiovascular disease and even death.

“This answers an important question in the HIV research and patient community,namely whether low level viremia is associated with persistent immune activation in patients being treated for HIV,” commented senior investigator Phyllis C. Tien, MD, an SFVAMC physician and an associate professor of medicine at UCSF.

The team examined blood specimens of nearly 1,116 HIV-infected subjects as part of the Study of Fat Redistribution and Metabolic Changes in HIV Infection. A new testing procedure by Roche Molecular Diagnostics that identifies the presence of virus below the limit of 20 copies per milliliter of blood was used as an assay.

As per the outcomes, the assay showed that low level viremia was apparently not associated with growing proportions of IL-6 or fibrinogen that are markers for inflammation and coagulation, respectively. Moreover, there seemed to be no co-relation between any level of virus and the existence of C-reactive protein which is a major indicator of inflammation or death risk.

The scientists believe that more than 10,000 copies per milliliter may lead to increased IL-6 and fibrinogen. Presumably, the more virus that is detectable and multiplying, the more are the chances of experiencing inflammation.

More researches to gauge other mechanisms involved in immune activation and inflammation that are unrelated to viral duplication ought to be worked on. The analysis is published in the journal, PloS One.