While alcohol abuse and biliary disease can result in the development of pancreatitis, the factors that contribute to the idiopathic form of the disease are not well understood. I propose that coxsackievirus infections account for a subset of cases of pancreatitis of unknown etiology. Evidence to support this concept is derived from serological studies, case reports and animal models. In reviewing the available data, it is obvious that the relationship between coxsackievirus infection and the development of pancreatitis is not a simple one. Many elements contribute to the development of the disease including the strain of the infecting virus, the genetic predisposition of the host and additional environmental factors that maintain the disease process. Studies that show an association between coxsackievirus infection and acute pancreatitis in humans are given additional support by the extensive data from mouse studies demonstrating that some serotypes (B4,B3) are tropic for the exocrine pancreas. Some viral strains may cause limited pancreatic tissue injury which is compatible with tissue repair followed by full restoration of pancreatic function. Other viral strains may cause more extensive tissue damage giving rise to chronic pancreatitis which, on a genetic background that predisposes to autoimmunity, may result in an autoimmune chronic pancreatitis. A multi-disciplinary approach is required to increase our understanding of the complex relationship between coxsackievirus infection and pancreatic diseases. Such studies should address the biology of viral replication, the immune response to infection, the role of viruses in the development of autoimmunity, the biology of pancreatic tissue injury and the underlying repair process.
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http://dx.doi.org/10.2741/a227 | DOI Listing |
Microorganisms
January 2025
The Stephan Angeloff Institute of Microbiology, Bulgarian Academy of Sciences, 1113 Sofia, Bulgaria.
Coxsackievirus B (CVB) infections, ranging from mild to severe diseases, lack specific antiviral treatments, underscoring the need for novel therapeutic strategies. Drug therapy is an important tool for controlling enterovirus infections, but clinically effective drugs do not currently exist, mainly due to the development of drug resistance. Combination therapy with two or more drugs has the potential to successfully inhibit viral infection more effectively than either drug alone as well as delay the development of resistance.
View Article and Find Full Text PDFJ Virol
January 2025
Centre for Heart Lung Innovation, St. Paul's Hospital, Vancouver, British Columbia, Canada.
Unlabelled: Enteroviruses cause nearly 1 billion global infections annually and are associated with a diverse array of human illnesses. Among these, myocarditis and the resulting chronic inflammation have been recognized as major contributing factors to virus-induced heart failure. Despite our growing understanding, very limited therapeutic strategies have been developed to address the pathological consequences of virus-induced chronic innate immune activation.
View Article and Find Full Text PDFAntiviral Res
January 2025
CAMS Key Laboratory of Antiviral Drug Research, Beijing Key Laboratory of Technology and Application for Anti-Infective New Drugs Research and Development, NHC Key Laboratory of Biotechnology of Antibiotics, Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China; State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. Electronic address:
Our previous study had found that cellular pseudokinase tribbles 3 (TRIB3) facilitates the infection of enterovirus A71 (EV-A71) via upregulating the protein level of EV-A71 receptor scavenger receptor class B member 2 (SCARB2). In the present study, we used metformin, which had been reported to down-regulate TRIB3 expression, to verify the potential of TRIB3 as an antiviral target. Here, we found that metformin can indeed impede the replication of EV-A71 and Coxsackievirus A16 (CVA16) through inhibiting the transcription of TRIB3 to indirectly down-regulate SCARB2 protein levels to block viral infection.
View Article and Find Full Text PDFVirol J
January 2025
State Key Laboratory of Vaccines for Infectious Diseases, Xiang An Biomedicine Laboratory, School of Life Sciences, School of Public Health, Xiamen University, Xiamen, 361102, PR China.
Coxsackievirus A6 (CVA6) has emerged as a major pathogen causing hand, foot and mouth disease (HFMD) outbreaks worldwide. The CVA6 epidemic poses a new challenge in HFMD control since there is currently no vaccine available against CVA6 infections. The Vero cell line has been widely used in vaccine production, particularly in the preparation of viral vaccines, including poliovirus vaccines and EV71 vaccines.
View Article and Find Full Text PDFmBio
January 2025
Shanghai Institute of Infectious Disease and Biosecurity, Fudan University, Shanghai, China.
Unlabelled: The KREMEN1 (KRM1) protein is a cellular receptor for multiple enteroviruses that cause hand, foot, and mouth disease (HFMD), including coxsackievirus CVA2, CVA3, CVA4, CVA5, CVA6, CVA10, and CVA12. The molecular basis for the broad recognition of these viruses by the KRM1 receptor remains unclear. Here, we report the indispensable role of the completely conserved VP2 capsid protein residue K140 (designated K2140) in mediating receptor recognition and infection by CVA10 and other KRM1-dependent enteroviruses.
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