The σ1 protein determines the extent of spread of reovirus from the gastrointestinal tract of mice

Kauffman, Robert S.; Wolf, Jacqueline L.; Finberg, Robert W.; Trier, Jerry S.; Fields, Bernard N.

doi:10.1016/0042-6822(83)90356-2

Cited by 71 publications

(66 citation statements)

References 15 publications

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“…After peroral inoculation, reovirus is thought to spread from Peyer's patches through lymphatics to regional lymph nodes and the bloodstream (5,44,45). From the bloodstream, virus gains access to sites of secondary replication (46).…”

Section: Resultsmentioning

confidence: 99%

“…The S1 gene also is associated with the capacity of reovirus to spread systemically from the enteric tract (4,5). After gastrointestinal infection, 3HA1, like T1L, spreads to sites of secondary replication, whereas 1HA3, like T3D, does not (5). The genetic determinants of viral replication and systemic dissemination from the murine lung are not known, although in a rat model, the S1 gene is linked to reovirus replication efficiency in the respiratory tract (6).…”

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confidence: 99%

“…In contrast, reassortant virus 1HA3, with nine gene segments from T1L and an S1 gene from T3D, fails to replicate to high titers at those sites, like T3D (2). The S1 gene also is associated with the capacity of reovirus to spread systemically from the enteric tract (4,5). After gastrointestinal infection, 3HA1, like T1L, spreads to sites of secondary replication, whereas 1HA3, like T3D, does not (5).…”

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confidence: 99%

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Genetic Determinants of Reovirus Pathogenesis in a Murine Model of Respiratory Infection

Nygaard

Lahti

Ikizler

et al. 2013

J Virol

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Many viruses invade mucosal surfaces to establish infection in the host. Some viruses are restricted to mucosal surfaces, whereas others disseminate to sites of secondary replication. Studies of strain-specific differences in reovirus mucosal infection and systemic dissemination have enhanced an understanding of viral determinants and molecular mechanisms that regulate viral pathogenesis. After peroral inoculation, reovirus strain type 1 Lang replicates to high titers in the intestine and spreads systemically, whereas strain type 3 Dearing (T3D) does not. These differences segregate with the viral S1 gene segment, which encodes attachment protein 1 and nonstructural protein 1s. In this study, we define genetic determinants that regulate reovirus-induced pathology following intranasal inoculation and respiratory infection. We report that two laboratory isolates of T3D, T3D C and T3D F , differ in the capacity to replicate in the respiratory tract and spread systemically; the T3D C isolate replicates to higher titers in the lungs and disseminates, while T3D F does not. Two nucleotide polymorphisms in the S1 gene influence these differences, and both S1 gene products are involved. T3D C amino acid polymorphisms in the tail and head domains of 1 protein influence the sensitivity of virions to protease-mediated loss of infectivity. The T3D C polymorphism at nucleotide 77, which leads to coding changes in both S1 gene products, promotes systemic dissemination from the respiratory tract. A 1s-null virus produces lower titers in the lung after intranasal inoculation and disseminates less efficiently to sites of secondary replication. These findings provide new insights into mechanisms underlying reovirus replication in the respiratory tract and systemic spread from the lung. Many viruses enter host organisms by invading mucosal surfaces, including those that line the respiratory tract. Infection by some pneumotropic viruses is restricted to the respiratory tract, whereas others replicate in the lung and disseminate to sites of secondary replication. Mammalian orthoreoviruses (reoviruses) naturally infect both the respiratory and gastrointestinal tracts (1). Reovirus strains differ in the capacity to replicate at mucosal sites and disseminate systemically. Studies of strain-specific differences in reovirus mucosal infection and systemic spread have enhanced an understanding of viral determinants and molecular mechanisms that regulate reovirus pathogenesis. For example, after peroral or intratracheal inoculation, reovirus strain type 1 Lang (T1L) replicates to higher titers than does strain type 3 Dearing (T3D) (2). This difference in replication efficiency at the site of primary replication segregates with the reovirus S1 gene segment (2, 3). Like T1L, reassortant virus 3HA1, with nine gene segments from T3D and an S1 gene from T1L, replicates to high titers in mucosal tissues (2). In contrast, reassortant virus 1HA3, with nine gene segments from T1L and an S1 gene from T3D, fails to replicate to high titers at those sit...

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Genetic Determinants of Reovirus Pathogenesis in a Murine Model of Respiratory Infection

Nygaard

Lahti

Ikizler

et al. 2013

J Virol

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“…Moreover, after oral inoculation, reovirus serotypes 1 and 3 adhere to the intestinal M cells (8,9) and are transported across these cells into the Peyer's patches. Infectious viruses are observed in mesenteric lymph nodes although their interaction with phagocytic cells has not been described (10).…”

mentioning

confidence: 98%

Rotavirus and reovirus interaction with mouse peritoneal resident phagocytic cells

Guimarães

Nozawa

Guimarães

et al. 1997

Braz J Med Biol Res

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Rotaviruses and reoviruses are involved in human and animal diseases. It is known that both viruses penetrate the gastrointestinal tract but their interaction with phagocytic cells is unknown. To study this interaction, peritoneal resident phagocytic cells were used and rotavirus and reovirus replication in peritoneal phagocytic cells was observed. However, rotavirus replication in these cells led to the production of defective particles since MA-104 cells inoculated with rotavirus phagocytic cell lysate did not show any evidence of virus replication. On the basis of these results, we suggest that, although reovirus dissemination may be helped by these phagocytic cells, these cells may control rotavirus infection and probably contribute to the prevention of its dissemination.

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“…In both cases, however, entry of the virus appears to occur through Peyer's patches, most likely via M cells [26]. Following oral infection, the virus may spread to mesenteric lymph nodes [27] and may disseminate and penetrate into many tissues, including the liver [28,29], pancreas [5,30], and endocrine tissues [31], as well as muscle [32] and heart tissue [33][34][35]. Age-associated susceptibility to reovirus serotype 3 leading to fatal encephalitis has been reported, the effect of which does not appear to be mediated by immunological factors but most likely reflect developmental conditions of neural tissues [36].…”

Section: Introductionmentioning

confidence: 99%

Experimental intestinal reovirus infection of mice

Montufar-Solis

Klein

2005

Immunol Res

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Reovirus, a member of the Reoviridae family, is a ubiquitous virus in vertebrate hosts. Although disease caused by reovirus infection is for the most part mild, studies of reovirus have been particularly valuable as a model for understanding the local host response to replicating foreign antigen in intestinal and respiratory sites. In this article, a brief overview is presented of the basic features of reovirus infection, as will the host's humoral and cellular immune response to during the infectious cycle. New information regarding the interactions and involvement of immune response molecules during reovirus infection will be presented based on multiple analyte array studies from our laboratory.

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The σ1 protein determines the extent of spread of reovirus from the gastrointestinal tract of mice

Cited by 71 publications

References 15 publications

Genetic Determinants of Reovirus Pathogenesis in a Murine Model of Respiratory Infection

Genetic Determinants of Reovirus Pathogenesis in a Murine Model of Respiratory Infection

Rotavirus and reovirus interaction with mouse peritoneal resident phagocytic cells

Experimental intestinal reovirus infection of mice

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