Jpn. J. Infect. Dis., 59 (2), 122-125, 2006
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Short Communication
Analysis of a Long-Term Discrepancy in Drug-Targeted Genes in Plasma HIV-1 RNA and PBMC HIV-1 DNA in the Same Patient
Shuzo Usuku*, Yuzo Noguchi, Mitsuo Sakamoto1, Takuya Adachi2, Hiroko Sagara2, Koji Sudo3, Masako Nishizawa4, Makiko Kondo3, Osamu Tochikubo5 and Mitsunobu Imai3
Department of Testing and Research, Yokohama City Institute of Health, Kanagawa 235-0012; 1The Jikei University School of Medicine, Tokyo 105-8461; 2Department of Infectious Diseases, Yokohama Municipal Citizen's Hospital, Kanagawa 240-8555; 3Microbiology Division, Kanagawa Prefectural Institute of Public Health, Kanagawa 253-0087; 4AIDS Research Center, National Institute of Infectious Diseases, Tokyo 208-0011; and 5Yokohama City University School of Medicine, Kanagawa 236-0004, Japan
(Received March 14, 2005. Accepted January 30, 2006)
*Corresponding author: Mailing address: Yokohama City Institute of Health, Takigashira 1-2-17, Isogo-ku, Yokohama City, Kanagawa 235-0012, Japan. Tel: +81-45-754-9804, Fax: +81-45-754-2210, E-mail: sh00-usuku@city.yokohama.jp
SUMMARY: Drug-resistance genotypes were investigated in a patient under treatment with anti-HIV drugs. Since the drug resistance-associated mutations in plasma HIV-1 RNA and proviral DNA in peripheral blood mononuclear cells (PBMCs) were inconsistent, changes were followed over time, and the discrepancy was shown to persist for a long period. In plasma HIV-1 RNA, D67N, K70R, T215Y, and Y188L were present in the reverse transcriptase (RT) region, and two primary mutations, I84V and L90M, were noted in the protease (Pro) region. In contrast, in proviral DNA, no drug resistance-associated mutations were found in the RT region, and mutations such as L90L/M were only infrequently present in the Pro region. This situation persisted for more than 3 years. In addition, sequencing analysis of the V3 loop in the envelope gene showed that non-syncytium-inducing/macrophage-tropic viruses contribute to acquisition of drug resistance. In this study, drug-resistant viruses were produced primarily at macrophages, and drug-sensitive viruses were maintained in PBMCs as a reservoir.