Hepatitis A: Viral Structure, Classification, Life Cycle, Clinical Symptoms, Diagnosis Error, and Vaccination

Figure 2

HAV replication cycle. At the hepatocyte’s basolateral membrane, the HAV virus interacts with host cell receptors, and its uncoated RNA is released into the cytoplasm. The cap-independent, IRES-driven translation of the positive-strand RNA genome produces polyproteins. Nonstructural proteins involved in genome replication (2B, 2C, 3AB, 3Dpol), the protease (3Cpro), and capsid proteins are produced by proteolytic processing of polyprotein. 2BC causes alterations in intracellular membranes, leading to the formation of a membrane-bound replicase complex that guides the production of a matching minus-strand RNA, which is subsequently employed as a template to make numerous new replicas of the RNA genome. Newly generated positive-strand RNAs are instructed to do more translation or RNA biosynthesis, or they can be packed into capsids to produce intracellular viral offspring. These freshly formed viral components are attracted to multivesicular bodies for eventual egress from infected cells into the biliary canaliculus or hepatic sinusoids via the apical plasma membrane and basolateral plasma membranes, respectively. The RNA genome is exposed after entering the cell, and the host ribosomes attach it to create polysomes. A viral RNA polymerase translation synthesizes viral particles that can be assembled and released into the biliary tree.