Cutting edge HIV research

Ground breaking research into the GB Virus type C (GBV-C, also referred to as hepatitis G virus) may impact on new approaches to treat and or prevent HIV infection and provide important insights to HIV pathogenesis that may be crucial for vaccine design according to Dr Aslam Sathar, medical scientist at the Nelson R Mandela School of Medicine. The study was under-taken with scientists from Iowa City VA Medical Center, and Departments of Internal Medicine, the University of Iowa, Iowa City, Iowa, USA.

Whilst the developed world experiences a decline in morbidity and mortality due to HIV, the HIV epidemic has yet to peak in KwaZulu-Natal. With no effective vaccine in sight, the data from this study suggests that African variants of GBV-C may influence HIV disease progression by inhibiting HIV replication via the induction of soluble factors, says Dr Sathar. In the epicenter of the HIV pandemic further such studies on the relation-ship between African variants of GBV-C and HIV are warranted.

GBV-C is a newly discovered virus which may have ancient African origins. GBV-C has not been conclusively associated with liver disease or any other clinical disease. It is a very common infection in humans, with approximately 10-20% of the general population in Africa actively infected. Because of shared modes of transmission, GBV-C co-infection occurs in 15%-43% of individuals with HIV infection. GBV-C isolates from around the world segregate into 5 distinct genotypes.

Genotype 2 is predominant in Western Europe and North America. GBV-C isolates in Africa are primarily genotypes 1 and 5, with the latter predominant in South Africa. Several studies conducted in Europe and North America of GBV-C co-infection among HIV-infected people report that those with GBV-C infection have higher CD4+ cell counts, lower HIV RNA levels, slower disease progression, prolonged survival and better response to treatment when com-pared to those without GBV-C. However, some studies have not found a significant difference between GBV-C infected and non-infected individuals.

In the laboratory it has been demonstrated that co-infection of cells with GBV-C genotype 2 and HIV results in the inhibition of HIV replication. This inhibition is mediated by soluble factors that are induced by GBV-C replication. Recently, in similar experiments undertaken by Dr Sathar in collaboration with scientists in the USA, African variants of GBV-C (genotypes 1 and 5) inhibited HIV replication. This inhibition correlated with the induction of soluble factors.