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Journal of Virology, January 2005, p. 860-868, Vol. 79, No. 2
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.2.860-868.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Human Immunodeficiency Virus Type 1 Clade B Superinfection: Evidence for Differential Immune Containment of Distinct Clade B Strains

Otto O. Yang,1* Eric S. Daar,2 Beth D. Jamieson,1 Arumugam Balamurugan,1 Davey M. Smith,3 Jacqueline A. Pitt,2 Christos J. Petropoulos,4 Douglas D. Richman,3,5,6 Susan J. Little,3 and Andrew J. Leigh Brown7

Department of Medicine, UCLA Medical Center,1 Los Angeles BioMedical Research Institute at Harbor-UCLA Medical Center and the David Geffen School of Medicine at UCLA, Los Angeles,2 Departments of Medicine,3 Pathology, University of California, San Diego,5 VA San Diego Healthcare System, La Jolla,6 ViroLogic, Inc., South San Francisco, California,4 Institute of Evolutionary Biology, School of Biological Sciences, University of Edinburgh, Edinburgh, Scotland7

Received 21 June 2004/ Accepted 4 September 2004

Sequential infection with different strains of human immunodeficiency virus type 1 (HIV-1) is a rarely identified phenomenon with important implications for immunopathogenesis and vaccine development. Here, we identify an individual whose good initial control of viremia was lost in association with reduced containment of a superinfecting strain. Subject 2030 presented with acute symptoms of HIV-1 infection with high viremia and an incomplete seroconversion as shown by Western blotting. A low set point of viremia (~1,000 HIV-1 copies/ml) was initially established without drug therapy, but a new higher set point (~40,000 HIV-1 copies/ml) manifested about 5 months after infection. Drug susceptibility testing demonstrated a multidrug-resistant virus initially but a fully sensitive virus after 5 months, and an analysis of pol genotypes showed that these were two phylogenetically distinct strains of virus (strains A and B). Replication capacity assays suggested that the outgrowth of strain B was not due to higher fitness conferred by pol, and env sequences indicated that the two strains had the same R5 coreceptor phenotype. Delineation of CD8+-T-lymphocyte responses against HIV-1 showed a striking pattern of decay of the initial cellular immune responses after superinfection, followed by some adaptation of targeting to new epitopes. An examination of targeted sequences suggested that differences in the recognized epitopes contributed to the poor immune containment of strain B. In conclusion, the rapid overgrowth of a superinfecting strain of HIV-1 of the same subtype raises major concerns for effective vaccine development.

* Corresponding author. Mailing address: 37-121 Center for Health Sciences, Division of Infectious Diseases, 10833 LeConte Ave., UCLA Medical Center, Los Angeles, CA 90095. Phone: (310) 794-9491. Fax: (310) 825-3632. E-mail: oyang{at}mednet.ucla.edu.

Journal of Virology, January 2005, p. 860-868, Vol. 79, No. 2
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.2.860-868.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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