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varicella (chickenpox) vaccine 737 vascular cell adhesion molecule 1 (VCAM-1)<br />

other conditions. HHV-3 may become latent when chickenpox<br />

resolves. Its DNA may become integrated into dorsal<br />

route ganglion cells. Varicella may be associated with the<br />

onset of herpes zoster or shingles later in life.<br />

varicella (chickenpox) vaccine<br />

An immunizing preparation comprised of attenuated varicella<br />

virus.<br />

varicella–zoster virus immunity<br />

Varicella–zoster virus (VZV) causes two illnesses: chickenpox<br />

or varicella and shingles or herpes zoster. Chicken-pox<br />

is the primary infection, and reactivation of the virus in<br />

adulthood causes shingles, a dermatomal exanthem. The<br />

immune response to chickenpox includes an IgM response<br />

at the end of the incubation period when a vesicular rash<br />

appears. Immunofluorescence can be used to detect VZVspecific<br />

antibodies reacting with the outer membranes of<br />

live VCV-infected cells. The initial antibodies are specific<br />

for VCV gB and are followed quickly by antibodies to<br />

gH and gE. Chickenpox patients also develop a cellular<br />

immune response that reacts with the same viral glycoproteins<br />

recognized by the antibody and a regulatory protein<br />

called IE62. Chickenpox patients develop lymphocyte<br />

proliferative responses to VZV gE, gI, gB, gH, and IE62<br />

antigens. CD8 + class I-restricted T cells and CD4 + class-IIrestricted<br />

T cells mediate VZV-specific cytotoxicity. The<br />

VZV cellular immune responses control the severity of<br />

the chickenpox exanthem in normal individuals. A latent<br />

VZV infection develops in most children, in whom the<br />

virus remains dormant in the dorsal root ganglia for many<br />

years. In senior adult years, the virus may become reactivated<br />

and induce herpes zoster (shingles) associated with<br />

the decreased immunity that accompanies increasing age.<br />

In the period prior to the development of zoster, anti-VZV<br />

glycoprotein antibody is greatly diminished in serum and<br />

cellular immunity is likewise decreased. Cells synthesizing<br />

IFN-γ (Th1 cells) diminish more than those producing<br />

interleukin-4 (IL4) (Th2 cells). Several weeks after the<br />

appearance of herpes zoster, high titers of VZV-specific<br />

antibody appear along with increased lymphoproliferative<br />

response to VZV antigens. Varicella–zoster immune globulin<br />

(VZIG) of high titer can prevent chickenpox if injected<br />

intermuscularly. It is important to give the globulin within<br />

3 to 4 days after exposure to chickenpox. A live attenuated<br />

varicella vaccine is available in the United States, Europe,<br />

and Japan. Vaccination is followed by the development of<br />

both humoral and cellular immune responses.<br />

variola (smallpox)<br />

Variola major is a Poxvirus variolae-induced disease that<br />

has been almost eliminated worldwide. This virus-induced<br />

disease causes vesicular and pustular skin lesions, leading<br />

to disfigurement, and produces viremia and toxemia. In<br />

the past, approximately one third of unvaccinated people<br />

succumbed to the disease. Variola minor (alastrim) is a mild<br />

form of smallpox produced by a different strain that is so<br />

weak it cannot induce the formation of pox on the chick<br />

chorioallantoic membrane. The term variola describes both<br />

the smallpox virus and the disease it causes.<br />

variolation (historical)<br />

The intracutaneous inoculation of pus from lesions of<br />

smallpox victims into healthy nonimmune subjects to<br />

produce smallpox immunity. In China, lesional crusts were<br />

ground to a powder and inserted into the nostrils. The<br />

procedure protected some individuals, but often caused<br />

life-threatening smallpox infections. Jenner’s introduction<br />

of cowpox vaccination to protect against smallpox rendered<br />

variolation obsolete.<br />

vascular addressins<br />

Mucin-like molecules on endothelial cells that bind selected<br />

leukocytes to certain anatomical sites. They govern the<br />

selective homing of leukocytes to specific locations. The<br />

cellular adhesion molecules on high endothelial venules<br />

(HEVs) facilitate extravasation of lymphocytes at particular<br />

anatomical sites. HEVs of the various lymphoid organs and<br />

tissues express different addressins on their surfaces and<br />

signal only lymphocytes with appropriate complementary<br />

homing receptors.<br />

VCAM<br />

Integrin-binding fragment of VCAM-1.<br />

ICAM-1<br />

Endothelial cell<br />

ICAM-2<br />

Vascular cell adhesion molecule 1 (VCAM-1).<br />

vascular cell adhesion molecule 1 (VCAM-1)<br />

A molecule that binds lymphocytes and monocytes. It is<br />

found on activated endothelial cells, dendritic cells, tissue<br />

macrophages, bone marrow fibroblasts, and myoblasts.<br />

VCAM-1 belongs to the immunoglobulin gene superfamily<br />

and is a ligand for VLA-4 (integrin α 4/β 1) and integrin<br />

α 4/β 7. It plays an important role in leukocyte recruitment<br />

to inflammatory sites; facilitates lymphocyte, eosinophil,<br />

and monocyte adhesion to activated endothelium; and<br />

participates in lymphocyte–dendritic cell interaction in the<br />

immune response.<br />

V

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