Abstract
SHIV-CN97001 played an important role in assessing the immune effect and strategy of the AIDS vaccine which included genes of the predominant prevalent HIV-1 strain in China. In this study, SHIV-CN97001 was in vivo passaged serially to construct pathogenic SHIV-CN97001/rhesus macaques model. To identify variation in the gp120 region of SHIV-CN97001 during passage, the fragments of gp120 gene were amplified by RT-PCR from the plasma of SHIV-CN97001 infected animals at the peak viral load time point and the gene distances (divergence, diversity) were calculated using DISTANCE. The analysis revealed that the genetic distances of SHIV-CN97001 in the third passage animals were the highest during in vivo passage. It had a relationship between viral divergence from the founder strain and viral replication ability. The nucleic acid sequence of the V3 region was highly conservative. All of the SHIV-CN97001 strains had V3 loop central motif (GPGQ) and were predicted to be using CCR5 co-receptor on the basis of the critical amino acids within V3 loop. These results show that there was no significant increase in the genetic distance during serial passage, and SHIV-CN97001 gp120 gene evolved toward ancestral states upon transmission to a new host. This could partly explain why there was no pathogenic viral strain obtained during in vivo passage.
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References
Balfe P, Shapiro S, Hsu M, et al. 2004. Expansion of quasispecies diversity but no evidence for adaptive evolution of SHIV during rapid serial transfers among seronegative macaques. Virology, 318: 267–279.
Harouse J M, Gettie A, Tan R C, et al. 1999. Distinct pathogenic sequela in rhesus macaques infected with CCR5 or CXCR4 utilizing SHIVs. Science, 284(5415): 816–819.
Herbeck J T, Nickle D C, Learn G H, et al. 2006. Human immunodeficiency virus type 1 env evolves toward ancestral states upon transmission to a new host. J Virol, 80(4): 1637–1644.
Kumar A, Lifson J D, Li Z, et al. 2001. Sequential immunization of macaques with two differentially attenuated vaccines induced long-term virus-specific immune responses and conferred protection against AIDS caused by heterologous simian human immunodeficiency Virus (SHIV(89.6)P). Virology, 279(1): 241–256.
Liang H, Wei M, Chen Z, et al. 2003. Sequence variation in the env V3–V4 region of HIV type 1 predominant subtype B and C strains circulating in China. Chinese J Exp Clin Virol, 17 (2), 153–158. (in Chinese)
Narayan S V, Mukherjee S, Jia F, et al. 1999. Characterization of a neutralization-escape variant of SHIVKU-1, a virus that causes acquired immune deficiency syndrome in pig-tailed macaques. Virology, 256(1): 54–63.
Nowak M A, Anderson R M, Mclean A R, et al. 1991. Antigenic diversity thresholds and the development of AIDS. Science, 254: 963–969.
Regina H L, Ryan K S, Vladimir L, et al. 2000. Sensitive and Robust One-Tube Real-Time Reverse Transcriptase-Polymerase Chain Reaction to Quantify SIV RNA Load: Comparison of One-versus Two-Enzyme Systems. AIDS, 16(13): 1247–1257.
Trichel A M, Rajakumar P A, Murphy-Corb M, et al. 2002. Species-specific variation in SIV disease progression between Chinese and Indian subspecies of rhesus macaque. J Med Primatol, 31: 171–178.
Ui M, Kuwata T, Igarashi T, et al. 1999. Protection of macaques against a SHIV with a homologous HIV-1 Env and a pathogenic SHIV-89.6P with a heterologous Env by vaccination with multiple gene-deleted SHIVs. Virology, 265(2): 252–263.
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Foundation items: CIPRA (U19 AI051915); 973 (2005CB-522903).
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Liu, Q., Yang, Gb., Ma, Y. et al. Sequence variation in the gp120 region of SHIV-CN97001 during in vivo passage. Virol. Sin. 23, 8–14 (2008). https://doi.org/10.1007/s12250-008-2892-4
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DOI: https://doi.org/10.1007/s12250-008-2892-4