• HIV-1 Superinfection: AE Subtype Supplanted by B Subtype (ThOrA1381)
  Authored by S. Jost, M.C. Bernard, L. Kaiser, S. Yerly, B. Hirschel, L. Goh, L. Perrin
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Dr. Jost and colleagues reported on an interesting case documenting a patient who developed a type B HIV infection after a type AE infection had already been established. One of the concerns about dual infection is the possibility of recombination and an expansion in HIV diversity. Previous studies in the laboratory and in animals have documented HIV recombination in the setting of dual infection. It is believed that superinfection with multiple clades in humans is unusual though the data is still limited.

The term "superinfection" relates to patients acquiring a second distinct strain of HIV in the setting of an already established HIV infection (some immunity develops during the period of primary infection). Previous reports of superinfection have suggested that the immune response to the second infection is improved so that control of viremia from the second viral strain is improved.

The study subject was a 38 year old who developed a primary infection syndrome in November 1998 (peak viral load = 805,000 and CD4+ count = 684 cells/mm³). He was enrolled in the QUEST trial (receiving amprenavir, abacavir, 3TC and AZT) for 18 months and then randomized to one of three therapeutic vaccine strategies along with six additional months of HAART. At that time the patient stopped therapy. The patient then took a vacation in Brazil, which included unprotected sex. He returned from the vacation and exhibited a pronounced increase in his viral level and a 300 cell decrease in CD4+ count. A clade analysis of the virus in his plasma revealed a type B virus while a clade analysis of his original strain revealed a type AE strain thus demonstrating superinfection with another virus. He developed that infection in the setting of low-level viremia presumably due to some level of immune control of his type AE virus. The growth capacity of the type B virus was higher than the original type AE virus.

Another interesting observation was that the original type AE strain could not be isolated from plasma after the type B infection was established but dual infection in some peripheral blood mononuclear cells could be demonstrated. The evaluation of this case was very elegant but the generalizability of the data is very unclear at present. This case report, along with the one presented by Bruce Walker on Wednesday (WeOrA197), is unsettling for the field of HIV vaccines. If these isolated reports are confirmed in larger numbers of HIV infected patients, the ability for an HIV vaccine to effectively prevent or control infection from additional viral strains seems to be a major hurdle.