Gangliosides as binding sites in SA-11 rotavirus infection of LLC-MK2 cells

Superti, Fabiana; Donelli, Gianfranco

doi:10.1099/0022-1317-72-10-2467

Cited by 67 publications

(51 citation statements)

References 26 publications

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“…After incubation for 3 h at 378C, cells were washed and further incubated in gentamicin-containing medium for 1 h. Rotavirus antigen synthesis was then assessed [36]. The addition of bacteria to virus-infected cells resulted in a noticeable inhibition of rotavirus replication (Fig.…”

Section: Virus Replication In Caco-2 Cells Post-incubated With Y Entmentioning

confidence: 99%

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Infection of human enterocyte-like cells with rotavirus enhances invasiveness of Yersinia enterocolitica and Y. pseudotuberculosis

Biase¹,

Petrone²,

Conte

et al. 2000

Journal of Medical Microbiology

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Mixed infection with rotavirus and either Yersinia enterocolitica or Y. pseudotuberculosis was analysed in Caco-2 cells, an enterocyte-like cell line highly susceptible to these pathogens. Results showed an increase of bacterial adhesion and internalisation in rotavirus-infected cells. Increased internalisation was also seen with Escherichia coli strain HB101 (pRI203), harbouring the inv gene from Y. pseudotuberculosis, which is involved in the invasion process of host cells. In contrast, the superinfection with bacteria of Caco-2 cells pre-infected with rotavirus resulted in decreased viral antigen synthesis. Transmission electron microscopy con®rmed the dual infection of enterocytes. These data suggest that rotavirus infection enhances the early interaction between host cell surfaces and enteroinvasive Yersinia spp.

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Section: Virus Replication In Caco-2 Cells Post-incubated With Y Entmentioning

confidence: 99%

“…Non-adsorbed viral particles were then removed by washing with PBS and fresh MEM without antibiotics was added for different time intervals before bacterial adhesion and invasion assays. In some experiments, intracytoplasmic rotavirus antigen synthesis was determined by indirect immuno¯uorescence [36].…”

Section: Viral Infectionmentioning

confidence: 99%

Infection of human enterocyte-like cells with rotavirus enhances invasiveness of Yersinia enterocolitica and Y. pseudotuberculosis

Biase¹,

Petrone²,

Conte

et al. 2000

Journal of Medical Microbiology

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“…While most animal rotaviruses require the presence of sialic acid on the cell surface for efficient binding and infectivity, this is not true of the human rotaviruses, nor of a few animal isolates (Fukudome et al, 1989 ;Keljo & Smith, 1988 ;Superti & Donelli, 1991 ;Rolsma et al, 1994). Me!…”

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confidence: 99%

Identification of mutations in the rotavirus protein VP4 that alter sialic-acid-dependent infection.

Ludert

Mason²,

Ángel

et al. 1998

Journal of General Virology

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To explore further the role of VP4 as the rotavirus cell attachment protein, VP7 monoreassortants derived from the sialic-acid-dependent simian strain RRV and from the sialic-acid-independent human strains D, DS-1 and ST-3 were tested for susceptibility of infectivity of neuraminidasetreated MA-104 cells. Infectivity of RRViD VP7 and RRViST-3 VP7 monoreassortants decreased when sialic acid was removed from the cell surface. However, of three separate RRViDS-1 VP7 monoreassortants tested, only one was sialic-aciddependent. Sequence analysis showed that both sialic-acid-independent strains contained a single amino acid change, Lys to Arg, at position 187. In addition, sialic-acid-independent infectivity was seen in one of 14 RRV VP4 neutralization escape mutants tested, and this strain was found to have a Gly to Glu change at amino acid position 150. These results indicate that positions 150 and 187 of VP4 play an important role in early rotavirus-cell interactions.The rotavirus virion is composed of three concentric layers of proteins and 11 segments of double-stranded RNA (Both et al., 1994 ;Estes, 1996). The outermost layer of the virion is comprised of two proteins, VP4 and VP7. VP4 forms dimeric spikes that project from the surface of the virion, which is constituted by VP7 (Shaw et al., 1993 ;Yeager et al., 1994).

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“…This restricted tissue-and cell-type-specific tropism is mediated by one or more specific host cell surface receptors that mediate rotavirus attachment. Numerous studies have implicated glycoconjugates (glycoproteins, glycolipids, and glycosphingolipids) as the putative rotavirus receptor(s) (4,19,32,34,41,55,58,59,66). A minority of animal rotaviruses require the presence of N-acetyl-neuraminic (sialic) acid (SA) residues on the cell surface for efficient binding and infectivity, but most animal and human rotaviruses are SA independent (13).…”

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confidence: 99%

VLA-2 (α2β1) Integrin Promotes Rotavirus Entry into Cells but Is Not Necessary for Rotavirus Attachment

Ciarlet

Crawford

Cheng

et al. 2002

J Virol

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In an attempt to identify the rotavirus receptor, we tested 46 cell lines of different species and tissue origins for susceptibility to infection by three N-acetyl-neuraminic (sialic) acid (SA)-dependent and five SA-independent rotavirus strains. Susceptibility to SA-dependent or SA-independent rotavirus infection varied depending on the cell line tested and the multiplicity of infection (MOI) used. Cells of renal or intestinal origin and transformed cell lines derived from breast, stomach, bone, or lung were all susceptible to rotavirus infection, indicating a wider host tissue range than previously appreciated. Chinese hamster ovary (CHO), baby hamster kidney (BHK-21), guinea pig colon (GPC-16), rat small intestine (Rie1), and mouse duodenum (MODE-K) cells were found to support only limited rotavirus replication even at MOIs of 100 or 500, but delivery of rotavirus particles into the cytoplasm by lipofection resulted in efficient rotavirus replication. The rotavirus cell attachment protein, the outer capsid spike protein VP4, contains the sequence GDE(A) recognized by the VLA-2 (␣2␤1) integrin, and to test if VLA-2 is involved in rotavirus attachment and entry, we measured infection in CHO cells that lack VLA-2 and CHO cells transfected with the human ␣2 subunit (CHO␣2) or with both the human ␣2 and ␤1 subunits (CHO␣2␤1) of VLA-2. Infection by SA-dependent or SA-independent rotavirus strains was 2-to 10-fold more productive in VLA-2-expressing CHO cells than in parental CHO cells, and the increased susceptibility to infection was blocked with anti-VLA-2 antibody. However, the levels of binding of rotavirus to CHO, CHO␣2, and CHO␣2␤1 cells were equivalent and were not increased over binding to susceptible monkey kidney (MA104) cells or human colonic adenocarcinoma (Caco-2, HT-29, and T-84) cells, and binding was not blocked by antibody to the human ␣2 subunit. Although the VLA-2 integrin promotes rotavirus infection in CHO cells, it is clear that the VLA-2 integrin alone is not responsible for rotavirus cell attachment and entry. Therefore, VLA-2 is not involved in the initial attachment of rotavirus to cells but may play a role at a postattachment level.

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Gangliosides as binding sites in SA-11 rotavirus infection of LLC-MK2 cells

Cited by 67 publications

References 26 publications

Infection of human enterocyte-like cells with rotavirus enhances invasiveness of Yersinia enterocolitica and Y. pseudotuberculosis

Infection of human enterocyte-like cells with rotavirus enhances invasiveness of Yersinia enterocolitica and Y. pseudotuberculosis

Identification of mutations in the rotavirus protein VP4 that alter sialic-acid-dependent infection.

VLA-2 (α2β1) Integrin Promotes Rotavirus Entry into Cells but Is Not Necessary for Rotavirus Attachment

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