title: Inverse relationship between viral load and genotypic resistance mutations in Korean patients with primary HIV type 1 infections.
abstract: The transmission of antiretroviral-resistant HIV-1 strains is associated with suboptimal virological responses to initial antiretroviral therapy. However, certain types of resistance mutations are known to be associated with decreased viral fitness, which confers a lower replication capacity than that of the wild-type virus in the absence of antiretroviral drugs. Therefore, we evaluated the relationship between antiretroviral resistance mutations and viral replication in the primary HIV-1 infection (PHI) period. From January 2002 to March 2005, 52 PHI patients were identified in the Republic of Korea. HIV-1 RNA genotyping was performed, and the resistance mutation score was obtained from the HIV Drug Resistance Database of Stanford University. We defined the sum of the average resistance mutation scores (SARMS) for each antiretroviral drug class as a measure of the degree of resistance of any specific strain. The overall mean SARMS was 2.00 +/- 2.74, and the annual mean did not change significantly during the study period. No critical resistance mutation gene was identified in the study group. The SARMS showed a weak negative correlation with the viral load log10 during PHI, but without statistical significance (r = -0.274, p = 0.051). But the mean SARMS of patients with a viral load exceeding 100,000 copies/ml was significantly lower than that of patients with a viral load of less than 100,000 copies/ml (p = 0.03). Evaluation of the potency of antiretroviral resistance revealed a weak negative correlation with viral replication in the PHI period. This could be one reason why the transmission of resistant strains in PHI patients is not increasing significantly despite the widespread use of highly active antiretroviral therapy (HAART).
authors.affiliation: Division of AIDS, Center for Immunology and Pathology, National Institute of Health, Seoul, Republic of Korea.
authors.forename: Bum Sik
authors.initials: BS
authors.lastname: Chin
authors.forename: Juyeon
authors.initials: J
authors.lastname: Choi
authors.forename: Jeong-Gu
authors.initials: JG
authors.lastname: Nam
authors.forename: Mee Kyung
authors.initials: MK
authors.lastname: Kee
authors.forename: Soon Deok
authors.initials: SD
authors.lastname: Suh
authors.forename: Jin Young
authors.initials: JY
authors.lastname: Choi
authors.forename: Chaeshin
authors.initials: C
authors.lastname: Chu
authors.forename: Sung Soon
authors.initials: SS
authors.lastname: Kim
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D024882:Drug Resistance, Viral / Q000235:genetics; D005260:Female; D005838:Genotype; D015658:HIV Infections / Q000821:virology*; D015497:HIV-1 / Q000187:drug effects* / Q000235:genetics*; D006801:Humans; D007723:Korea; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D009154:Mutation; D010802:Phylogeny; D019562:Viral Load