Arrrrrggggghhhhhh...... all those words, and no expansion on the key phrase, "three important viral markers". One of them is presumably a gp120 epitope, which would not be positive news for AGPH.
This still doesn't touch on the recent hints by Gallo, relating to a lack of progression in patients that have had a viral bounce after HAART.
Here's a recent abstract from Pittsburgh. I didn't spend any time looking for relevant hints regarding the additional two markers......
Virology 1998 Feb 15;241(2):251-259
Evolution of human immunodeficiency virus type 1 envelope sequences in
infected individuals with differing disease progression profiles.
Shankarappa R, Gupta P, Learn GH Jr, Rodrigo AG, Rinaldo CR Jr, Gorry MC, Mullins JI, Nara PL, Ehrlich GD
Department of Pathology, University of Pittsburgh, Pennsylvania 15261, USA.
Sequence variation displayed by the human immunodeficiency virus type 1 (HIV-1) has been proposed to be linked to the
pathogenesis of acquired immunodeficiency syndrome (AIDS). To assess viral evolution during the course of infection, we
evaluated sequence variability in the env variable domains in four HIV-1-infected individuals exhibiting differing profiles of
CD4+ T cell decline when followed from seroconversion until the development of AIDS or loss of followup. Proviral
sequences encoding the V3-V5 region of gp 120 were obtained following PCR amplification of peripheral blood mononuclear
cell DNA and cloning. Virus in each patient was relatively homogeneous early in infection and then diverged with time, more
consistently at its nonsynonymous sites. Just prior to or coincident with a rapid decline in CD4+ T cell numbers, sequences
were found with basic amino acid substitutions clustered within and downstream of the gp 120 V3 domain. Within the
constraints of the current data set, we conclude that the virus appears to continually accumulate changes in its amino acid
sequences well into the time of marked CD4+ T cell decline. |
