Biomedical Engineering Reference
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Initial binding of the virus to cell surface glycosaminoglycans (gags), primar-
ily heparin and dermatan sulfate mediated by glycoproteins C (gC) and B (gB)
[188,189] , is followed by specific interactions between gD and identified receptors
(HveM herpes virus entry mediators) HveA and HveC. HveC belongs to the immu-
noglobulin superfamily and is highly expressed in the nervous system [190] . In order,
attachment to GAGs are generally followed by specific interactions with HVEMs
that lead to fusion of the virus envelope with the cell surface membrane and entry of
the viral capsid with its surrounding tegument proteins into the cell. The mechanism
of viral penetration into the cell is not well understood, but it requires multiple gly-
coproteins (gB, gH/gL, and gD) [190] .
5.5.1.4 Replication
Following infection of a cell, the herpes virus proteins produced are called
1. immediate-early phase
2. early phase
3. late phase.
Another research study using flow cytometry on a member of the herpes virus
family, KSHV, indicates the possibility of an additional lytic stage called delayed-
late phase. All these stages of lytic infection, particularly late lytic , are more distinct
from the latency stage. In HSV-1, no protein products are detected during latency,
but they are detected during the lytic cycle ( Fig. 5.11 ).
The function of early proteins transcribed is generally to regulate genetic replica-
tion of the virus. On entering the cell, an -TIF protein joins the viral particle and
aids in immediate-early transcription. The virion host shutting off protein (VHS or
UL41) is crucial for viral replication. This enzyme shuts off protein synthesis in the
HSV lytic replication
Release
Translation
γ
β
α
Binding and entry
α TIF
Nuclear
binding
Transcription
Assembly
DNA Synthesis
Figure 5.11 HSV lytic replication.
 
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