BACKGROUND/AIMS: Co-infection with hepatitis B virus (HBV) and hepatitis C virus (HCV) increases the risk of development and the severity of chronic liver disease. Although dominant and suppressive effects of each virus over the other have been reported in vivo, in vitro studies of HBV/HCV co-infection have been limited to analysis of the effects of over-expression of HCV proteins on HBV replication. METHODS: We have re-examined HBV/HCV interactions in Huh-7 cells following co-infection with cell culture-propagated HCV (HCVcc; genotype 2a) and a recombinant adenovirus vector capable of delivering a replication-competent HBV genome (AdHBV; genotype A). RESULTS: While intracellular HCV RNA levels were significantly increased when cells were pre-infected with AdHBV, HCV replication and virion secretion were not altered by simultaneous infection with AdHBV or AdHBV superinfection of HCV-infected cells. Likewise intracellular and secreted HBV DNA levels and HBV promoter activities were either unchanged or modestly increased by HCVcc infection. Despite this, HCV E2 and HBsAg proteins colocalized extensively in co-infected cells suggesting shared stages in viral egress. CONCLUSIONS: These studies indicate that there is little direct interaction of HBV and HCV in co-infected hepatocytes and imply that indirect effects of host-viral interactions dictate viral dominance in HBV/HCV co-infected individuals.
BACKGROUND/AIMS: Co-infection with hepatitis B virus (HBV) and hepatitis C virus (HCV) increases the risk of development and the severity of chronic liver disease. Although dominant and suppressive effects of each virus over the other have been reported in vivo, in vitro studies of HBV/HCV co-infection have been limited to analysis of the effects of over-expression of HCV proteins on HBV replication. METHODS: We have re-examined HBV/HCV interactions in Huh-7 cells following co-infection with cell culture-propagated HCV (HCVcc; genotype 2a) and a recombinant adenovirus vector capable of delivering a replication-competent HBV genome (AdHBV; genotype A). RESULTS: While intracellular HCV RNA levels were significantly increased when cells were pre-infected with AdHBV, HCV replication and virion secretion were not altered by simultaneous infection with AdHBV or AdHBV superinfection of HCV-infected cells. Likewise intracellular and secreted HBV DNA levels and HBV promoter activities were either unchanged or modestly increased by HCVcc infection. Despite this, HCV E2 and HBsAg proteins colocalized extensively in co-infected cells suggesting shared stages in viral egress. CONCLUSIONS: These studies indicate that there is little direct interaction of HBV and HCV in co-infected hepatocytes and imply that indirect effects of host-viral interactions dictate viral dominance in HBV/HCV co-infected individuals.
Authors: Zhaochun Chen; Giacomo Diaz; Teresa Pollicino; Huaying Zhao; Ronald E Engle; Peter Schuck; Chen-Hsiang Shen; Fausto Zamboni; Zhifeng Long; Juraj Kabat; Davide De Battista; Kevin W Bock; Ian N Moore; Kurt Wollenberg; Cinque Soto; Sugantha Govindarajan; Peter D Kwong; David E Kleiner; Robert H Purcell; Patrizia Farci Journal: Proc Natl Acad Sci U S A Date: 2018-11-12 Impact factor: 11.205
Authors: Pankaj Puri; Anil C Anand; Vivek A Saraswat; Subrat K Acharya; Shiv K Sarin; Radha K Dhiman; Rakesh Aggarwal; Shivaram P Singh; Deepak Amarapurkar; Anil Arora; Mohinish Chhabra; Kamal Chetri; Gourdas Choudhuri; Vinod K Dixit; Ajay Duseja; Ajay K Jain; Dharmesh Kapoor; Premashis Kar; Abraham Koshy; Ashish Kumar; Kaushal Madan; Sri P Misra; Mohan V G Prasad; Aabha Nagral; Amarendra S Puri; R Jeyamani; Sanjiv Saigal; Samir Shah; Praveen K Sharma; Ajit Sood; Sandeep Thareja; Manav Wadhawan Journal: J Clin Exp Hepatol Date: 2014-06-24