Role of Ca2+in the replication and pathogenesis of rotavirus and other viral infections

Ruiz, Marie Christine; Cohen, Jean; Michelangeli, Fabián A.

doi:10.1054/ceca.2000.0142

Cited by 98 publications

(87 citation statements)

References 100 publications

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“…The up-regulation of several calcium-related genes in WSSV infection may be a compensating reaction of the host genes. Basically, Ca 2+ plays a key role in many pathological processes, including viral infections (19). In summary of this and previously reported studies, different gene expression profiles are observed in response to WSSV and YHV, suggesting different host immune responses to the two pathogenic viruses.…”

Section: Expression Profiling Of Genes Responsive To Yellow Head Virusupporting

confidence: 64%

Differentially expressed genes in Penaeus monodon hemocytes following infection with yellow head virus

Pongsomboon¹,

Tang²,

Boonda³

et al. 2008

BMB Reports

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Section: Expression Profiling Of Genes Responsive To Yellow Head Virusupporting

confidence: 64%

Differentially expressed genes in Penaeus monodon hemocytes following infection with yellow head virus

Pongsomboon¹,

Tang²,

Boonda³

et al. 2008

BMB Reports

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“…These changes may in turn lead to cell death (29,31) and also may be ultimately related to pathogenesis. The synthesis de novo of viral proteins is required for these alterations to take place (24).…”

Section: Discussionmentioning

confidence: 99%

Silencing of Rotavirus NSP4 or VP7 Expression Reduces Alterations in Ca ²⁺ Homeostasis Induced by Infection of Cultured Cells

Zambrano¹,

Díaz

Peña

et al. 2008

J Virol

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Rotavirus infection of cells in culture induces major changes in Ca2؉ homeostasis. These changes include increases in plasma membrane Ca 2؉ permeability, cytosolic Ca 2؉ concentration, and total cell Ca 2؉ content and a reduction in the amount of Ca 2؉ released from intracellular pools sensitive to agonists. Various lines of evidence suggest that the nonstructural glycoprotein NSP4 and possibly the major outer capsid glycoprotein VP7 are responsible for these effects. In order to evaluate the functional roles of NSP4 and other rotavirus proteins in the changes in Ca 2؉ homeostasis observed in infected cells, the expressions of NSP4, VP7, and VP4 were silenced using the short interfering RNA (siRNA) technique. The transfection of specific siRNAs resulted in a strong and specific reduction of the expression of NSP4, VP7, and VP4 and decreased the yield of new viral progeny by more than 90%. Using fura-2 loaded cells, we observed that knocking down the expression of NSP4 totally prevented the increase in Ca 2؉ permeability of the plasma membrane and cytosolic Ca 2؉ concentration measured in infected cells. A reduction in the levels of VP7 expression partially reduced the effect of infection on plasma membrane Ca 2؉ permeability and Ca 2؉ pools released by agonist (ATP). In addition, the increase of total Ca 2؉ content (as measured by 45 Ca 2؉ uptake) observed in infected cells was reduced to the levels in mock-infected cells when NSP4 and VP7 were silenced. Finally, when the expression of VP4 was silenced, none of the disturbances of Ca 2؉ homeostasis caused by rotaviruses in infected cells were affected. These data altogether indicate that NSP4 is the main protein responsible for the changes in Ca 2؉ homeostasis observed in rotavirus-infected cultured cells. Nevertheless, VP7 may contribute to these effects. Viral-associated diarrhea remains one of the most common causes of morbidity and mortality among infants and young children. Worldwide estimations indicate that rotaviruses are the leading viral agent associated with severe diarrhea in children younger than 5 years old (20). In addition, rotavirus infections are also a main cause of diarrhea in calves, piglets, and the young of other animals of economic importance (20). Thus, further knowledge of the virus-cell interactions and the events leading to pathogenesis are necessary to improve or develop new strategies that may prevent or reduce the health and economic impact caused by rotavirus infections.Rotaviruses are members of the Reoviridae family. The rotavirus virion is icosahedral, nonenveloped, and composed of three concentric layers of proteins and a genome of 11 segments of double-stranded RNA. Each genomic segment, with the exception of segment 11, encodes one viral protein for a total of six structural (VP1 to VP7) and six nonstructural proteins (NSP1 to NSP6). The inner layer of the virion is formed by VP2 and also contains the RNA-dependent RNA polymerase VP1 and the guanylyltransferase/methylase VP3. The middle capsid is composed of the major virion...

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“…Rotavirus infection of cultured cells induces a progressive rise in the cytosolic Ca 2ϩ concentration (5,31,46,48). This increase may be involved in rotavirus-induced apoptosis, and indeed, the intracellular calcium ion chelator BAPTA-AM partially inhibits apoptosis (7).…”

Section: Discussionmentioning

confidence: 99%

Bax Is Activated during Rotavirus-Induced Apoptosis through the Mitochondrial Pathway

Martin‐Latil

Mousson

Autret

et al. 2007

J Virol

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Rotaviruses are the leading cause of infantile viral gastroenteritis worldwide. Mature enterocytes of the small intestine infected by rotavirus undergo apoptosis, and their replacement by less differentiated dividing cells probably leads to defective absorptive function of the intestinal epithelium, which, in turn, contributes to osmotic diarrhea and rotavirus pathogenesis. Here we show that infection of MA104 cells by the simian rhesus rotavirus strain RRV induced caspase-3 activation, DNA fragmentation, and cleavage of poly(ADP-ribose) polymerase; all three phenomena are features of apoptosis. RRV induced the release of cytochrome c from mitochondria to the cytosol, indicating that the mitochondrial apoptotic pathway was activated. RRV infection of MA104 cells activated Bax, a proapoptotic member of the Bcl-2 family, as revealed by its conformational change. Most importantly, Bax-specific small interfering RNAs partially inhibited cytochrome c release in RRV-infected cells. Thus, mitochondrial dysfunction induced by rotavirus is Bax dependent. Apoptosis presumably leads to impaired intestinal functions, so our findings contribute to improving our understanding of rotavirus pathogenesis at the cellular level.

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Role of Ca2+in the replication and pathogenesis of rotavirus and other viral infections

Cited by 98 publications

References 100 publications

Differentially expressed genes in Penaeus monodon hemocytes following infection with yellow head virus

Differentially expressed genes in Penaeus monodon hemocytes following infection with yellow head virus

Silencing of Rotavirus NSP4 or VP7 Expression Reduces Alterations in Ca ²⁺ Homeostasis Induced by Infection of Cultured Cells

Bax Is Activated during Rotavirus-Induced Apoptosis through the Mitochondrial Pathway

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Role of Ca2+in the replication and pathogenesis of rotavirus and other viral infections

Cited by 98 publications

References 100 publications

Differentially expressed genes in Penaeus monodon hemocytes following infection with yellow head virus

Differentially expressed genes in Penaeus monodon hemocytes following infection with yellow head virus

Silencing of Rotavirus NSP4 or VP7 Expression Reduces Alterations in Ca 2+ Homeostasis Induced by Infection of Cultured Cells

Bax Is Activated during Rotavirus-Induced Apoptosis through the Mitochondrial Pathway

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Silencing of Rotavirus NSP4 or VP7 Expression Reduces Alterations in Ca ²⁺ Homeostasis Induced by Infection of Cultured Cells