interaction, giving access to the virus to enter the host cell. The virus binds

first to the host cell surface. This binding is mediated by the recognition of

specific protein sequences present on the host cell surface by the viral

glycoproteins.

2. Internalization: After the attachment is established through receptor

binding, the virus is taken into the host cell cytoplasm. This could be

through direct fusion (fusion of viral envelope and host cellular mem-

brane) or through receptor-mediated endocytosis (followed by most

viruses). The entry of the virus into the host cell is commonly dependent

on receptor-mediated endocytosis. In this process, the virus particle is

engulfed by the host cell membrane, which then fuses with the intracellular

compartments, known as endosomes. Consequently, the virus is released

inside the endosomal lumen. Generally, “substances” taken up by the

endosomes, ultimately end up in lysosomes, degraded by some hydrolytic

enzymes. But most viruses can escape this degradation process.

The most common way of viral internalization is through clathrin-

mediated endocytosis (CME). This process requires a protein coat to be

assembled on the membrane to induce membrane curvature and form a

spherical invagination. Along with clathrin, which is a scaffolding protein,

other factors like epsin, ampiphisin, adaptor protein 2, dynamin, actin, and

PIP2 are also important in the process of CME [6]. These proteins as-

semble and form a complex on the cytoplasmic side of the plasma

membrane, which leads to the formation of a coat at the site of en-

docytosis. The phospholipid PIP2 is found at a higher concentration at the

FIGURE 2.7 HSV-1 infection cycle: HSV-1 latency period and reactivation from latency

in neurons.

Introduction to basic virology

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