Host cell pathways required for early Cytomegalovirus replication

Host cell pathways required for early Cytomegalovirus (CMV) replication represent the collective cellular machinery and metabolic processes that the virus exploits to establish infection and initiate genome synthesis. Upon entry, CMV induces a profound metabolic shift known as metabolic reprogramming, significantly increasing glucose uptake and flux through the fatty acid synthesis pathway to provide lipids for viral envelopes (Munger et al., 2008). The virus also hijacks the host's PI3K/Akt/mTOR signaling pathway to ensure robust protein translation and to prevent the cell from undergoing stress-induced apoptosis or autophagy (Buchkovich et al., 2008). Early replication is further dependent on the host's cell cycle control mechanisms, where CMV manipulates cyclin-dependent kinases (CDKs) to create an S-phase-like environment conducive to viral DNA replication (Moorman et al., 2001). Additionally, the virus utilizes host nuclear import and export proteins to transport viral genomes and regulatory proteins between the cytoplasm and the nucleus. Because these pathways are fundamental to host cell survival, drugs targeting them, such as mTOR inhibitors or metabolic antagonists, must be carefully dosed to avoid systemic toxicity. Research into these host factors is driven by the need for host-directed therapies that might be less susceptible to the rapid mutational resistance seen with traditional direct-acting antivirals (Jean Beltran et al., 2016).

Other names

HCMV host dependency factorsHost-virus interactomeCMV host cell requirementsHost factors for Cytomegalovirus replication

Inhibition of essential host metabolic or signaling pathways to restrict the cellular environment necessary for viral genome replication and protein synthesis.