Inefficient fusion due to a lack of attachment receptor/co-receptor restricts productive human immunodeficiency virus type 1 infection in human hepatoma Huh7.5 cells.
Since the widespread use of the highly active antiretroviral therapy, the incidence of liver disease has increased to become a leading cause of death among human immunodeficiency virus type 1 (HIV-1)-infected individuals. It can be proposed that the ability of HIV-1 to infect hepatocytes could influence liver diseases. Although the presence of HIV-1 was identified in hepatocytes from HIV-1 seropositive patients, the susceptibility of hepatocytes to HIV-1 infection in vitro remains controversial. We present evidence here that human hepatoma cells are not productively infected with CD4-dependent HIV-1 strains because of inefficient fusion related to an absence of cell surface CD4 and CXCR4. However, these cells display an increased susceptibility to infection with a CD4-independent viral isolate through an interaction with galactosyl ceramide, an alternate receptor for HIV-1. This study provides further understanding of the susceptibility of human hepatocytes to HIV-1 infection. However, in vivo investigations are recommended to consolidate these data.
Centre de Recherche en Infectiologie, Université Laval, Québec, QC G1V 4G2, Canada.
Rémi
R
Fromentin
Mélanie R
MR
Tardif
Michel J
MJ
Tremblay
D015704:CD4 Antigens / Q000096:biosynthesis; D002460:Cell Line; D005699:Galactosylceramides / Q000096:biosynthesis; D015870:Gene Expression; D015497:HIV-1 / Q000254:growth & development / Q000472:pathogenicity / Q000502:physiology*; D022781:Hepatocytes / Q000821:virology*; D006801:Humans; D019718:Receptors, CXCR4 / Q000096:biosynthesis; D015728:Receptors, HIV / Q000096:biosynthesis*; D053585:Virus Attachment
D015704:CD4 Antigens; C527276:CXCR4 protein, human; D005699:Galactosylceramides; D019718:Receptors, CXCR4; D015728:Receptors, HIV