Molecular Biology of the Cell by Bruce Alberts, Alexander Johnson, Julian Lewis, David Morgan, Martin Raff, Keith Roberts, Peter Walter by by Bruce Alberts, Alexander Johnson, Julian Lewis, David Morg

CELL BIOLOGY OF INFECTION
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nucleocapsid
(A)
outer membrane of
nuclear envelope
nucleus
nucleus
inner membrane of
nuclear envelope
(?)
Golgi
viral DNA
endoplasmic
reticulum
WRAPPING
Golgi
cisterna
CYTOSOL
intracellular enveloped
virion (3 membranes)
intracellular mature
virion (1 membrane)
plasma
membrane
FUSION
WITH
PLASMA
MEMBRANE
EXTRACELLULAR
SPACE
extracellular
enveloped
virion
(2 membranes)
Figure 23–27 Complex strategies for
viral envelope acquisition. (A) Herpesvirus
nucleocapsids assemble in the nucleus
and then bud through the inner nuclear
membrane into the space between the
inner and outer nuclear membranes,
acquiring a lipid bilayer membrane coat.
The virus particles then apparently lose this
coat when they fuse with the endoplasmic
reticulum membrane to escape into the
cytosol. Subsequently, the nucleocapsids
bud into the Golgi apparatus and bud
out again on the other side, thereby
acquiring two new membrane coats in
the process. The virus then buds from
the cell surface with a single membrane
when its outer membrane fuses with the
plasma membrane. (B) Vaccinia virus
(which is closely related to the virus that
causes smallpox and is used to vaccinate
against smallpox) assembles in “replication
factories” in the cytosol, far away from the
plasma membrane. The immature virion,
with one membrane, is then surrounded
by two additional membranes, both
acquired from the Golgi apparatus by a
poorly understood wrapping mechanism,
to form the intracellular enveloped virion.
After fusion of the outermost membrane
with the host-cell plasma membrane, the
extracellular enveloped virion is released
from the host cell.
(B)
immature virion
(1 membrane)
CYTOSOL
EXTRACELLULAR
SPACE
Several bacteria that replicate in the host cell’s cytosol have adopted a remarkable
mechanism that depends on actin polymerization for movement. These
bacteria include the human pathogens Listeria monocytogenes, Shigella flexneri,
Rickettsia rickettsii (which causes Rocky Mountain spotted fever), and Burkholderia
pseudomallei (which causes melioidosis, a disease characterized by severe
respiratory symptoms). Baculovirus, an insect virus, also uses this mechanism for
intracellular movement. All of these pathogens induce the nucleation and assembly
of host-cell actin filaments at one pole of the bacterium or virus. The growing
filaments generate force and push the pathogens through the cytosol at rates of
up to 1 μm/sec (Figure 23–28). New filaments form at the rear of each pathogen
and are left behind like a rocket trail as the microbe advances; the filaments
MBoC6 m24.35/23.27
depolymerize within a minute or so as they encounter depolymerizing factors in
the cytosol. For L. monocytogenes and S. flexneri, the moving bacteria collide with
the plasma membrane and move outward, inducing the formation of long, thin,
host-cell protrusions with the bacteria at their tip. As shown in Figure 23–28, a
neighboring cell often engulfs these projections, allowing the bacteria to enter the
neighbor’s cytoplasm without exposure to the extracellular environment, thereby
avoiding antibodies produced by the host’s adaptive immune system. For B. pseudomallei,
movement and collision of the bacteria with the plasma membrane promotes
cell–cell fusion, which serves a similar purpose of immune avoidance while
allowing continued bacterial replication.