The H9N2 low pathogenic avian influenza (LPAI) viruses have often caused moderate mortality with severe clinical signs in domestic poultry in many Eurasian countries and have occasionally caused clinical respiratory diseases in humans, but the basis for their pathogenesis remains unclear especially in chickens. To better understand the effect of immunosuppression on the risk of H9N2 viral infection, the pathogenesis and host immune responses of the H9N2 LPAI virus in a T-cell-suppressed chicken model were investigated. Cyclosporin A (CsA) treatment led to suppression of cell-mediated immunity such as CD8+ T-cells and reduced expression of IFN-gamma mRNA. T-cell suppression correlated with high viral load in the oropharynx and cloaca of H9N2 LPAI virus-infected specific pathogen free (SPF) chickens. Elevated level of viral RNA in the peripheral blood lymphocytes was found only in immunocompromised chickens. Viral protein and associated cellular apoptosis were observed only in the kidney of the immunocompromised chickens, particularly in those that had died. Our findings suggest that T-cell-mediated responses are important in influenza viral clearance and may help to explain in part the reasons for the increased mortality in chickens infected with H9N2 LPAI viruses in domestic poultry farms.
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http://dx.doi.org/10.1016/j.virusres.2007.12.019 | DOI Listing |
Access Microbiol
November 2024
Departamento de Microbiologia, Universidade Federal de Viçosa (UFV), Av. Peter Henry Rolfs, Viçosa, 36570-900, Minas Gerais, Brazil.
Cureus
October 2024
Department of Infectious Diseases, Al Jalila Children's Specialty Hospital, Dubai, ARE.
J Med Case Rep
November 2024
Division of Pediatric Infectious Diseases, Memorial Care Miller Children's & Women's Hospital Long Beach, Clinical Professor of Pediatrics, University of California Irvine Department of Pediatrics, Irvine, CA, USA.
Background: Histoplasma is a fungal pathogen found in many parts of the world. In North America, its distribution is traditionally thought to be endemic to the Ohio and Mississippi River valleys. Development of histoplasmosis after Histoplasma exposure is related to degree of inoculum exposure and susceptibility, for example, immunocompromised status.
View Article and Find Full Text PDFAm J Transplant
January 2025
Ömura Satoshi Memorial Institute, Laboratory of Virus Infection, Kitasato University, Tokyo, Japan.
Recently, live-attenuated measles, rubella, varicella, and mumps vaccines have been administered to carefully selected post-liver transplant patients. Although attention has been focused on post-vaccination antibody titers and adverse events, the real-life clinical benefits remain unclear. A comprehensive analysis of breakthrough infections and natural boosters (asymptomatic cases with significant elevation in virus antibody titers) following immunization post-liver transplantation was conducted from 2002-2023, exploring the timing, frequency, correlation with domestic outbreaks, and degree of antibody elevation.
View Article and Find Full Text PDFCureus
June 2024
Oral Medicine and Radiology, Sharad Pawar Dental College and Hospital, Datta Meghe Institute of Higher Education and Research, Wardha, IND.
The varicella-zoster virus reactivates to cause the "herpes zoster" (HZ). ''Varicella-zoster virus'' (VZV) termed as ''HHV-3'' or ''human herpesvirus-3'' infection causes herpes zoster. Varicella, the primary form of the virus, is chickenpox, and the secondary form of the virus is herpes zoster also called shingles.
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