Clade B HIV-1 superinfection with wild-type virus after primary infection with drug-resistant clade B virus

Abstract

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.

Dynamics of HIV Type 1 Recombination Following Superinfection

“…Others have reported dual infection 10 or superinfection 3,5,6 with the same subtype followed by recombination. Koelsch et al 11 described complete replacement of drug-resistant virus with superinfecting wild-type virus, while Pingen et al 12 described complete replacement of wildtype virus with drug-resistant virus, but recombination was not detected in these reports.…”

Socioeconomic Impact of HIV/AIDS on Households under Free Antiretroviral Therapy in Preah Sihanouk Province, Cambodia

“…Therefore, it is likely that the susceptibility to superinfection is higher during the first year following primary infection, when HIV-1-specific humoral immunity is not fully developed, and the discrepancies between the abovementioned studies might be explained by differences in the time elapsed between the initial and the second infection. This hypothesis is supported by initial observations in HIV-2-infected macaques, which can only become productively superinfected by a distinct HIV-2 virus within 8 weeks following primary infection [22], and by a substantial percentage of documented superinfections that occurred within one year of primary HIV-1 infection in humans [11,30,31,33,34].…”

“…Since then, multiple reported cases have described interclade [10,11,[23][24][25][26][27][28][29] as well as intraclade [9,[30][31][32][33][34][35] superinfections, but also triple superinfections [28,32,36], or superinfections involving substantially divergent strains belonging to the different HIV-1 and HIV-2 groups [37,38].…”

“…Studies report an overall poor control of the superinfecting virus, which is in most cases associated with a sudden increase in viral load and accelerated disease progression [9][10][11]26,[28][29][30][31][32][33][34]42,60,66,67]. While this could be attributed to a loss of immunemediated control due to a lack of overlap in crucial epitopes between the two HIV-1 strains, it has also been suggested that superinfection preferentially occurs in individuals initially infected with HIV-1 strains displaying a reduced fitness compared to the superinfecting virus [68].…”

“…While this could be attributed to a loss of immunemediated control due to a lack of overlap in crucial epitopes between the two HIV-1 strains, it has also been suggested that superinfection preferentially occurs in individuals initially infected with HIV-1 strains displaying a reduced fitness compared to the superinfecting virus [68]. For instance, in the absence of antiretroviral treatment, it has been shown that upon superinfection, wild-type HIV-1 strains can outgrow drug-resistant variants displaying reduced replication capacity [31,33,34,67]. Importantly, sudden increases in viral loads might have allowed detection of a significant number of HIV-1 superinfections described thus far, and therefore it is not excluded that less fit and/ or less pathogenic superinfecting strains never outgrow the initial virus and remain unnoticed minority variants with no significant impact on disease progression.…”