UPF1 is Crucial for the Infectivity of Human Immunodeficiency Virus type 1 Progeny Virions

Student Author(s)

Anna Kristina Serquina

UMMS Affiliation

Program in Gene Function and Expression; Program in Molecular Medicine; Department of Biochemistry and Molecular Pharmacology

Publication Date


Document Type



Immunology of Infectious Disease | Virology


The SF1 helicase MOV10 is an antiviral factor that is incorporated into human immunodeficiency virus type 1 (HIV-1) virions. We now report that HIV-1 virions also incorporate UPF1, which belongs to the same SF1 helicase subfamily as MOV10 and functions in the nonsense-mediated decay (NMD) pathway. Unlike ectopic MOV10, the overexpression of UPF1 does not impair the infectivity of HIV-1 progeny virions. However, UPF1 becomes a potent inhibitor of HIV-1 progeny virion infectivity when residues required for its helicase activity are mutated. In contrast, equivalent mutations abolish the antiviral activity of MOV10. Importantly, cells depleted of endogenous UPF1, but not of another NMD core component, produce HIV-1 virions of substantially lower specific infectivity. The defect is at the level of reverse transcription, the same stage of the HIV-1 life cycle inhibited by ectopic MOV10. Thus, whereas ectopic MOV10 restricts HIV-1 replication, the related UPF1 helicase functions as a cofactor at an early post-entry step.

DOI of Published Version



Serquiña AK, Das SR, Popova E, Ojelabi OA, Roy CK, Göttlinger HG. UPF1 is crucial for the infectivity of human immunodeficiency virus type 1 progeny virions. J Virol. 2013 Aug;87(16):8853-61. doi: 10.1128/JVI.00925-13. Link to article on publisher's website

Journal/Book/Conference Title

Journal of virology

Related Resources

Link to article in PubMed

PubMed ID