Expert
Reviews in Molecular Medicine: http://www.expertreviews.org/
Accession information: (99)00066-6h.htm (shortcode: fig004cso); 4 May 1999
Request PDF version Back to
main article
Assembly of vaccinia virus in a human cell
Christopher M. Sanderson and Geoffrey L. Smith

Figure 4. Assembly of vaccinia virus
in a human cell. SER = smooth endoplasmic reticulum; RER = rough endoplasmic
reticulum. The assembly of vaccinia virus is a complex process that results
in the formation of two infectious forms of virus: intracellular mature virus
(IMV) and extracellular enveloped virus (EEV). (a) Vaccinia-virus morphogenesis
starts in cytoplasmic factories with the formation of membrane
crescents, which extend to form spherical immature virus (IV) particles. (b)
IV particles are non-infectious until they undergo morphological condensation
into brick-shaped IMV particles. IMV particles recruit the virus
A27L protein (p14 kDa) onto their surface. (c) During infection, most IMV
particles remain within the cell until they are released by cell lysis. However,
some IMV particles become enveloped by membranes derived from either the trans-Golgi
network (TGN) or tubular endosomes (d) to form intracellular enveloped virus
(IEV) (e). (f) Proteins within the outer membrane of IEV particles induce
the polarised, unidirectional polymerisation of actin, which propels the particle
towards the plasma membrane and assists the infection of neighbouring cells.
(g) During this process, the outer membrane of the IEV particle fuses with
the plasma membrane of the cell, exposing an infectious particle on the cell
surface and leaving proteins that induce actin polymerisation within the plasma
membrane. (h) If these particles remain attached to the cell they are called
cell-associated enveloped virus (CEV); (i) however, if they are released from
the cell they are called extracellular enveloped virus (EEV). (j) In addition
to the classical mechanism of vaccinia-virus assembly described above, EEV
particles can also form via direct budding of IMV particles through the plasma
membrane. This alternative mechanism of EEV formation might be facilitated
by the transport of viral glycoproteins from the TGN to the plasma membrane
(k) (fig004cso).
| home
| search | glossary
| links | sitemap
| contact |
Expert Reviews
in Molecular Medicine © Cambridge University
Press ISSN 1462-3994 (Disclaimer and copyright)
Editorial Office: Centre for Applied Research
in Educational Technologies (CARET), 1st Floor, 16 Mill Lane, Cambridge,
CB2 1SB, UK. Tel: +44 (0)1223 765 375; Fax: +44(0)1223 765 505; E-mail: ermm@caret.cam.ac.uk