Mutation of the HIV-1 virus, and the presence of more than one subtype of HIV in a single individual, are but two of the impediments in the development of an effective anti-HIV vaccine.

It is well-known that error processes in viral replication generate mutations of HIV-1. These can occur as point mutations at a particular locus on a gene, as hypermutations with up to 700 substitutions for each round of replication, or as recombination which usually results in about three errors per round of replication.

The problems encountered by patients consequent on recombination were highlighted in a session on HIV pathogenesis.

Multiple variants occur within the same cell, with recombinants being found both in individuals and at epidemic levels. Variants of SIV have been found within 15 days of primary infection.

Andreas Meyerhans of the Department of Virology, University of Saarland, described an investigation of the splenocytes of two splenectomised patients, in which multiple divergent viruses were found. More than 75% of the infected splenocytes contained two or more variants, with a mean of three to four per cell. Both recombinant and parent variants were seen in the same cell.

The distribution was remarkably similar in the two patients, despite different clinical and virological settings. An extraordinary degree of diversity was observed: up to 29% amino acid difference and numerous recombinants were evident. Recombination profoundly influences HIV evolution and presents a huge challenge to analysts.

Multiple proviruses within the same cell is the norm, not the exception, said Meyerhans. Most CD4 cells have two to four provirus copies. Multiple variants and recombinants suggest that rampant recombination is taking place.

This observation carries consequences for standard phylogenetic analysis. It also results in a broadening of immune recognition and it may help the emergence of multiple drug resistant HIV variants.

AIDS 2002 Conference News produced by Health & Development Networks/Key Correspondent Team