Role of R5 phenotypic variation in mother-to-child transmission of HIV-1

Mariangela Cavarelli¹, Ingrid Karlsson², Marisa Zanchetta³, Liselotte Antonsson⁴, Anna Plebani⁵, Carlo Giaquinto⁶, Eva Maria Fenyö², Anita De Rossi³ and Gabriella Scarlatti¹

¹Viral Evolution and Transmission Unit, DIBIT, Fondazione Centro San Raffaele, Milan, 20132, Italy

²Division of Medical Microbiology/Virology, Department of Laboratory Medicine, Lund University, Lund, 223 62, Sweden

³Department of Oncology and Surgical Sciences, Unit of Viral Oncology, AIDS Reference Center, University of Padova, IOV-IRCCS, Padova, 35022, Italy

⁴Division of Cellular and Molecular Pharmacology, Department of Experimental Medical Science, Lund University, Lund, 223 62, Sweden

⁵Department of Pediatrics, University of Milan, Clinica De Marchi, Milan, 20122, Italy

⁶Department of Pediatrics, University of Padova, 35022, Italy

corresponding author email

from Fourth Dominique Dormont International Conference. Host-Pathogen Interactions in Chronic Infections
Paris, France. 13-15 December 2007

Retrovirology 2008, 5(Suppl 1):O2doi:10.1186/1742-4690-5-S1-O2


Published:	9 April 2008

First paragraph (this article has no abstract)

R5 viruses were shown to have an intrinsic phenotypic variation, as demonstrated by their capacity to differentially infect in vitro target cells expressing CCR5/CXCR4 chimeric receptors [1,2]. In this study we have explored the hypothesis that the phenotypic variation of R5 viruses of pregnant women could play a role in mother-to-child transmission (MTCT) of HIV-1.