My current research interests are focused on the following areas: mechanisms of reverse transcription and recombination; RNA packaging and virus assembly; and interactions between distinct viruses. Retroviral RNA is reverse transcribed to generate viral DNA that integrates into the host genome to form the provirus. Currently, many of the antiretroviral drugs target the step of reverse transcription in the viral life cycle. Recombination occurs frequently during reverse transcription; this process can reassort mutations and increase the variation in the viral population. It has been demonstrated that viral strains with multiple drug resistance can be generated by recombination from strains that are resistant to a single drug. Using in vivo systems, my laboratory is dissecting the mechanisms of reverse transcription and retroviral recombination to gain a better understanding of these very important processes. Retroviruses package their RNA into viral particles specifically through interactions between the viral Gag polyprotein and a region in the viral RNA termed the packaging signal. My laboratory observed that murine leukemia virus (MLV) and spleen necrosis virus (SNV), an avian retrovirus, have a nonreciprocal recognition between their Gag polyproteins and packaging signals. SNV proteins can package RNA containing either the SNV or MLV packaging signal, whereas MLV proteins can package only RNA with the MLV packaging signal. My laboratory is dissecting the cis- and trans-acting elements important for this specific recognition. Using MLV and SNV as model systems, my laboratory observed that viral RNA from distinct viruses can be packaged into a single virion. Furthermore, recombinant retroviruses can be generated from these two viruses. This is the first experiment demonstrating that genetic interaction can occur between distinct retroviruses. My laboratory is currently examining the mechanisms and limitations of these interactions.

National Institute of Health (NIH)
Division of Clinical Sciences - NCI (NCI)
Intramural Research (Z01)
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Clinical Sciences
United States
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Majerciak, Vladimir; Pripuzova, Natalia; McCoy, J Philip et al. (2007) Targeted disruption of Kaposi's sarcoma-associated herpesvirus ORF57 in the viral genome is detrimental for the expression of ORF59, K8alpha, and K8.1 and the production of infectious virus. J Virol 81:1062-71
Haque, Muzammel; Wang, Victoria; Davis, David A et al. (2006) Genetic organization and hypoxic activation of the Kaposi's sarcoma-associated herpesvirus ORF34-37 gene cluster. J Virol 80:7037-51
Tang, Shuang; Tao, Mingfang; McCoy Jr, J Philip et al. (2006) The E7 oncoprotein is translated from spliced E6*I transcripts in high-risk human papillomavirus type 16- or type 18-positive cervical cancer cell lines via translation reinitiation. J Virol 80:4249-63
Majerciak, Vladimir; Yamanegi, Koji; Nie, Sarah H et al. (2006) Structural and functional analyses of Kaposi sarcoma-associated herpesvirus ORF57 nuclear localization signals in living cells. J Biol Chem 281:28365-78
Tang, S; Tao, M; McCoy Jr, J P et al. (2006) Short-term induction and long-term suppression of HPV16 oncogene silencing by RNA interference in cervical cancer cells. Oncogene 25:2094-104
Zheng, Zhi-Ming; Baker, Carl C (2006) Papillomavirus genome structure, expression, and post-transcriptional regulation. Front Biosci 11:2286-302
Zheng, Zhi-Ming; Tang, Shuang; Tao, Mingfang (2005) Development of resistance to RNAi in mammalian cells. Ann N Y Acad Sci 1058:105-18
Bodaghi, Sohrab; Yamanegi, Koji; Xiao, Shu-Yuan et al. (2005) Colorectal papillomavirus infection in patients with colorectal cancer. Clin Cancer Res 11:2862-7
Yamanegi, Koji; Tang, Shuang; Zheng, Zhi-Ming (2005) Kaposi's sarcoma-associated herpesvirus K8beta is derived from a spliced intermediate of K8 pre-mRNA and antagonizes K8alpha (K-bZIP) to induce p21 and p53 and blocks K8alpha-CDK2 interaction. J Virol 79:14207-21
Bodaghi, Sohrab; Wood, Lauren V; Roby, Gregg et al. (2005) Could human papillomaviruses be spread through blood? J Clin Microbiol 43:5428-34

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