APOBEC3G genotypes and proviral DNA hypermutations on HIV/AIDS disease progression in Thai and Cambodian children

Author:

Bunupuradah Torsak1,Matsuoka Kazuhiro2,Imahashi Mayumi2,Iwatani Yasumasa23,Ananworanich Jintanat145,Puthanakit Thanyawee16,Saphonn Vonthanak7,Aurpibul Linda8,Sophonphan Jiratchaya1,Yagi Tetsuya9,Phanuphak Praphan1,Sugiura Wataru2310

Affiliation:

1. HIV-NAT, the Thai Red Cross AIDS Research Centre, 104 Ratchadamri Road, Pathumwan, Bangkok 10330, Thailand

2. Clinical Research Center, National Hospital Organization Nagoya MedicalCenter, 4-1-1 Sannomaru, Naka-ku, Nagoya, Aichi 460-0001, Japan

3. Program in Integrated Molecular Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Aichi 466-8550, Japan

4. Current address: US Military HIV Research Program, Henry M. Jackson Foundation for the Advancement of Military Medicine, 6720 A, Rockledge Drive, Suite 400, Bethesda, MD 20817, USA

5. SEARCH, the Thai Red Cross AIDS Research Centre, 104 Ratchadamri Road, Pathumwan, Bangkok, 10330, Thailand

6. Department of Pediatrics, Faculty of Medicine, Chulalongkorn University, 1873, Rama IV Road, Pathumwan, Bangkok, Thailand 10330

7. Social Health Clinic, #2, St 289 (Kim Il Sung Blvd), Khan Toul Kok, Phnom Penh, Cambodia

8. Research Institute for Health Sciences, Chiang Mai University, 110 Intavaroros Road, Sriphum, Muang, Chiang Mai, 50200, Thailand

9. Department of Infectious Diseases, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Aichi 466-8550, Japan

10. GlaxoSmithKline KK, 6-15, Sendagaya 4-chome, Shibuya-ku, Zip: 151-8566, Tokyo, Japan

Abstract

Aim: To evaluate the effect of APOBEC3G host factor on HIV/AIDS progression in perinatally HIV-infected Thai and Cambodian children with distinct clinical patterns; rapid progressors (RPs) and long-term nonprogressors (LTNPs). Materials & methods: APOBEC3G genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism in DNA samples. APOBEC3G-mediated G-to-A hypermutations were analyzed by sequencing of the vif/vpu genes from proviral DNA. Results: Frequency of APOBEC3G 186H/R genotypes, AA:AG:GG, in the RPs was 100:0:0% and 83:17:0% (p = 0.3) in LTNPs. Hypermutation of the vif-coding region was observed in none of the RPs and 8.3% of LTNPs (p = 0.5). Hypermutations at the vpu genes were not detected in either groups’ proviral DNA. Conclusion: We observed no significant association of APOBEC3G genotypes and hypermutation rates between children with different profiles of HIV/AIDS disease progression.

Publisher

Future Medicine Ltd

Subject

Virology

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