Clade B HIV-1 superinfection with wild-type virus after primary infection with drug-resistant clade B virus.
BACKGROUND
The immunological response to HIV-1 infection has been postulated to impede superinfection with a second virus; however, a few recent reports have documented cases of HIV-1 superinfection in humans either from different viral clades or from the same clade.


OBJECTIVE
To differentiate between co-infection and superinfection in a patient harboring a distinct wild-type HIV 4 months after primary infection with drug-resistant HIV.


METHODS
Detailed dye primer and clonal sequencing along with length polymorphism analysis was used to investigate the evolutionary linkage between viral populations sampled at different timepoints.


RESULTS
After a set point viral load of -6000 copies HIV RNA/ml, the viral load jumped to 34 000 copies/ml at month 4 and, shortly after, to almost 200 000 copies/ml. At that time a second viral strain was first detected by dye primer sequencing of a pol fragment. These findings were confirmed by analysis of a 1300 bp gag-pol fragment and clonal sequencing and phylogenetic analysis of the V3 region. Length polymorphism analysis of the gp120 V4-V5 region showed that the second viral population was absent even as a minority population until month 4, when it was found to be the majority population, and the initial variant was present only as a minority. Both strains were subtype B.


CONCLUSIONS
These data support intraclade HIV-1 superinfection by wild-type virus in the absence of antiretroviral therapy in a patient initially infected with drug-resistant HIV. The substantially different in-vivo viral growth characteristics observed illustrate the potential for superinfection to impact disease progression.
Koelsch
Kersten K
KK
University of California San Diego, La Jolla, CA 92093, USA. kkoelsch@uscd.edu
Smith
Davey M
DM
Little
Susan J
SJ
Ignacio
Caroline C
CC
Macaranas
Theresa R
TR
Brown
Andrew J
AJ
Petropoulos
Christos J
CJ
Richman
Douglas D
DD
Wong
Joseph K
JK
D004279:DNA, Viral / Q000032:analysis; D024882:Drug Resistance, Viral; D015658:HIV Infections / Q000188:drug therapy / Q000235:genetics* / Q000276:immunology; D015497:HIV-1; D006801:Humans; D012367:RNA, Viral / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015163:Superinfection / Q000235:genetics* / Q000276:immunology; D019562:Viral Load
D004279:DNA, Viral; D012367:RNA, Viral