site of endocytosis, where it can interact with multiple membrane proteins.

Electron micrograph studies have shown CME pits with well-defined

clathrin lattice forming the backbone of the budding vesicle [7].

3. Uncoating: To gain access to the cytoplasm, the virus needs to be released

from the endosome. Indeed, the low pH of the endosomal vesicle induces

conformational changes of the viral glycoprotein, inducing the fusion of

the virus envelope and the endosomal membrane. Following this fusion

event, in some cases, there is an activation of the viral ion channel. Proton

pumps of the endosomal membrane regulate the low pH of the endosomes.

This pH initiates the fusion between the viral envelope and the endosomal

membrane, which is a determinant step of the infection cycle. At this

acidic pH, the viral glycoprotein undergoes a conformational change,

followed by the process which induces the merging of the viral membrane

with that of the endosome of the host. This process also results in for-

mation of some fusion pores, which facilitate the transfer of the viral

genome into the host cell cytosol.

4. Viral gene expression and genome replication: The viral genome re-

plication depends on the type of genome as discussed earlier. For the

genome replication and transcription, some of the virus families may per-

form it independently without the need of the host cell machinery. However,

all the viruses absolutely depend on the host translation machinery, i.e., the

ribosomes for their protein synthesis without an exception.

5. Assembly and budding: In the case of enveloped viruses, assembly and

budding are the final steps of the virus replication, before the release of

infectious progeny virions. Most of the viruses are not in favor of forming

a long-term stable host-virus relationship inside the infected host. The sur-

vival of these viruses depends on host-to-host transmission, which, in turn,

depends on the release of the progeny virus from the infected host cell. They

might take the advantage of the lipid rafts present in the cell membrane of

infected cells as site of assembly and budding of the neosynthesized virion

[8–10] Lipid rafts are membrane domains of variable size, enriched in

cholesterol and sphingolipids [11]. Lipid rafts have been described in the

budding process of viruses such as human immunodeficiency virus-1 (HIV-1),

influenza virus, and Ebola virus [11–14]. To form an infectious virion, at

least one copy of each vRNA should be packaged. For example, in case of

the influenza A virus, one copy of each of the eight segments must be

present to form an infectious particle. This infectious particle should have

the ability to infect and enter a host cell but would replicate depending on

the access to host cellular factors. This process starts with capsid assembly

followed by genome packaging. A packaging signal present on the viral

genome is specifically recognized by the viral capsid which does selective

packaging of the viral genome.

6. Release: There are different strategies followed by viruses to be released

from the host cell. First, they could get released by cell lysis. In this case,

there is no specific mechanism being followed except the host cell

membrane being disrupted by the accumulation of viral proteins and

Introduction to basic virology

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