enzymes. Second, for enveloped viruses, the capsid gets coated by the host

lipid bilayer before the virus release. This could go through two different

mechanisms: i) the lipid bilayer coating can occur after the capsid as-

sembly has taken place. This needs the interaction between the viral capsid

and its glycoproteins present on the envelop. ii) The lipid bilayer coating

can occur simultaneously with the capsid assembly, as seen in retroviruses.

Following the lipid bilayer coating around the viral capsid, the host cell plasma

membrane must undergo conformational changes, resulting in the formation of a bud-

like structure that facilitates the extracellular release of the virion. This process is

commonly called “budding” of the newly formed viral particles. Most of the viruses

have one peptide motif or a domain that triggers this budding process. These viral

proteins contain the specific peptide motif or domain interact with various host cel-

lular factors such as members of small GTPases or actin family to regulate the for-

mation of the bud, ultimately releasing the virion. For example, viruses like HIV-1

and Ebola virus use the Endosomal sorting complex required for transport (ESCRT)

complex to achieve membrane scission and subsequent release of the newly formed

virus depends on VPS4 protein [15,16]. This process is mediated by the late domain

sequences present in viral proteins (p6 for Gag of HIV-1) that recruit the ESCRT-I

and ESCRT-II complex at the site of budding (Figures 2.8 and 2.9).

2.4

VIRUS-HOST INTERACTIONS

As discussed earlier, the virus requires access to the host cellular machinery for its

survival, specifically for the translation of viral proteins. Hence, there is an absolute

need for the virus to interact with the host cell and its various components.

Moreover, the parameters of an infection depend on the virus involved as well as

FIGURE 2.9 Budding and release mechanism of an enveloped virus.

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Bioprocessing of Viral Vaccines