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Chickenpox01:20

Chickenpox

Chickenpox is an acute, highly contagious disease caused by the varicella-zoster virus (VZV), a double-stranded DNA virus belonging to the Herpesviridae family. Its transmission occurs primarily through the inhalation of respiratory droplets or direct contact with vesicular fluid from skin lesions. The incubation period typically ranges from 10 to 21 days, during which the virus replicates and disseminates through sequential phases within the host. Although generally self-limiting in children,...
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Smallpox is a severe contagious disease caused by the Variola major virus, a double-stranded DNA member of the Poxviridae family.Variola major transmission occurs primarily via inhalation of virus-laden droplets or direct contact with infectious scabs. The incubation period averages approximately seven days, although it may range from 7 to 17 days depending on the inoculum and host factors.Clinically, the prodromal phase is marked by an abrupt onset of high fever, malaise, headache, and myalgia.
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
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Cytomegalovirus (CMV) disease is caused by human cytomegalovirus, a double-stranded DNA virus of the Herpesviridae family. While primary CMV infection is often asymptomatic in immunocompetent individuals, the virus can cause severe disease in neonates and immunocompromised patients. CMV is the most common cause of congenital viral infection in the United States, and a major pathogen in solid organ and hematopoietic stem cell transplant recipients.CMV is transmitted via bodily fluids, sexual...
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Poliomyelitis is caused by poliovirus, a small, non-enveloped, positive-sense RNA virus of the Picornaviridae family and Enterovirus genus. Transmission occurs primarily via the fecal-oral route, often through ingestion of contaminated water or food. The virus initially replicates in the oropharynx and intestinal mucosa, particularly in lymphoid tissues such as the tonsils, Peyer’s patches, and regional lymph nodes. Primary viremia follows, allowing dissemination throughout the body.In most...

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Simian varicella virus pathogenesis.

Ravi Mahalingam1, Ilhem Messaoudi, Don Gilden

  • 1Departments of Neurology, University of Colorado Denver School of Medicine, Aurora, CO 80045, USA. ravi.mahalingam@ucdenver.edu

Current Topics in Microbiology and Immunology
|February 27, 2010
PubMed
Summary
This summary is machine-generated.

Simian varicella virus (SVV) in nonhuman primates offers a valuable model for studying varicella zoster virus (VZV) pathogenesis, latency, and reactivation. Experimental immunosuppression in SVV-infected monkeys mimics zoster, aiding research into immune responses.

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Evaluation of Zika Virus-specific T-cell Responses in Immunoprivileged Organs of Infected Ifnar1-/- Mice

Published on: October 17, 2018

Area of Science:

  • Virology
  • Immunology
  • Primate Models

Background:

  • Varicella zoster virus (VZV) exclusively infects humans, necessitating animal models for research.
  • Simian varicella virus (SVV) shares pathological, virological, and immunological similarities with VZV.
  • Understanding VZV latency and reactivation is crucial for developing effective treatments.

Purpose of the Study:

  • To establish and validate nonhuman primate models for studying VZV pathogenesis, latency, and reactivation.
  • To investigate the viral and immunological aspects of SVV infection in various primate species.
  • To explore the role of adaptive immunity in modulating VZV reactivation.

Main Methods:

  • Utilizing natural SVV infection in cynomolgus and African green monkeys.
  • Employing intrabronchial inoculation of rhesus macaques with SVV.
  • Inducing experimental immunosuppression in latently SVV-infected monkeys.

Main Results:

  • SVV infection in nonhuman primates recapitulates key features of human VZV infection.
  • Both natural and experimental SVV infections provide robust models for studying viral latency and host immune responses.
  • Experimental immunosuppression of latently infected monkeys led to zoster, demonstrating a model for reactivation studies.

Conclusions:

  • Nonhuman primate models infected with SVV are highly effective for studying VZV pathogenesis, latency, and reactivation.
  • These models facilitate research into the complex interplay between the host immune system and viral reactivation.
  • The SVV-macaque model of zoster offers new insights into how immune deficiency impacts virus reactivation.