Replication of Arboviruses in Arthropod in Vitro Systems: An Overview

Pudney, Mary; Leake, C. J.; Buckley, Sonja M.

doi:10.1016/b978-0-12-470290-5.50011-3

Cited by 15 publications

(5 citation statements)

References 63 publications

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“…Since it is known that the MMVP 12 medium has a higher osmotic pressure than L-15 medium and this has been associated with differences in the induction of cytopathic effects [18], the effect of MMVP 12 on FFWI by JE-Sar was investigated. In MMVP 12 medium, syncytium formation was almost totally inhibited, and it proved possible to propagate the infected cell line as though it was not infected.…”

Section: Comparison Of Cell Fusing Capacity Of Je-bei and Je-sarmentioning

confidence: 99%

Differences in fusogenicity and mouse neurovirulence of Japanese encephalitis viruses

Higgs

Gould

1991

Archives of Virology

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The fusogenic capacity in AP-61 cell monolayers of 10 strains of Japanese encephalitis (JE) virus from different geographic locations was compared. One strain, isolated from Beijing (JE-Bei), did not fuse AP-61 cells after replication (fusion from within; FFWI), whereas all other strains fused these cells by 72 h post-infection. JE-Bei also readily established a non-cytolytic persistent infection in AP-61 cells. Differences in the envelope proteins of fusogenic and non-fusogenic virus were detected by haemagglutination-inhibition tests and by antigenic analysis using monoclonal antibodies. Yields of infectious virus in either AP-61 or Vero cell cultures were similar if JE-Bei was compared with the fusogenic strain (JE-Sar) but yields of haemagglutinin were 50-100 fold higher with the non-fusogenic virus, implying excessive generation of non-infectious particles. When added directly to AP-61 cell monolayers at pH6, only JE-Bei produced significant fusion from without (FFWO) presumably reflecting the larger quantity of antigen. Cell monolayers persistently infected with JE-Bei or monolayers treated with UV-inactivated JE-Bei, were resistant to superinfection with JE, West Nile and dengue 2 viruses but were susceptible to infection with the alphavirus Sindbis. When administered intracerebrally (I/C) to newborn and weanling mice, the viruses were equally neurovirulent. However, fusogenic JE-Sar was significantly more neurovirulent than JE-Bei for weanling mice after intraperitoneal (I/P) or subcutaneous (S/C) inoculation. Mice given non-fusogenic JE-Bei, resisted the peritoneal challenge with fusogenic JE-Sar, and West Nile but not Semliki Forest virus when given 6 h after the first virus. The potential significance of cell fusion by JE virus and interference through over production of non-infectious virus, is discussed in the context of JE virus virulence.

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Section: Comparison Of Cell Fusing Capacity Of Je-bei and Je-sarmentioning

confidence: 99%

Differences in fusogenicity and mouse neurovirulence of Japanese encephalitis viruses

Higgs

Gould

1991

Archives of Virology

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“…The main representatives are the widely distributed human pathogen Crimean-Congo hemorrhagic fever virus (CCHFV), which causes severe and often fatal hemorrhagic fever in humans (16), and the Nairobi sheep disease virus, which circulates in Africa and Asia (23) and induces acute and fatal hemorrhagic gastroenteritis in sheep and goats. Although nairovirus infection in vertebrate cells has been documented (for reviews, see references 36 and 38), there are only a few reports concerning nairovirus infection in their tick vector or in tick cells (31).…”

mentioning

confidence: 99%

Nairovirus RNA Sequences Expressed by a Semliki Forest Virus Replicon Induce RNA Interference in Tick Cells

Garcia

Billecocq

Crance³

et al. 2005

J Virol

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We report the successful infection of the cell line ISE6 derived from Ixodes scapularis tick embryos by the tick-borne Hazara virus (HAZV), a nairovirus in the family Bunyaviridae. Using a recombinant Semliki Forest alphavirus replicon that replicates in these cells, we were able to inhibit replication of HAZV, and we showed that this blockage is mediated by the replication of the Semliki Forest alphavirus replicon; the vector containing the HAZV nucleoprotein gene in sense or antisense orientation efficiently inhibited HAZV replication. Moreover, expression of a distantly related nucleoprotein gene from Crimean-Congo hemorrhagic fever nairovirus failed to induce HAZV silencing, indicating that the inhibition is sequence specific. The resistance of these cells to replicate HAZV correlated with the detection of specific RNase activity and 21-to 24-nucleotide-long small interfering RNAs. Altogether, these results strongly suggest that pathogen-derived resistance can be established in the tick cells via a mechanism of RNA interference.

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“…Phleboviruses tested (Pacui, Sandfly fever Sicilian a n d Sandfly fever Naples), none was shown to multiply in mosquito or tick cells in vitro (9). The Phlebovirus Toscana (TOS), isolated in I t a l y from sandflies, was n o r m a l l y cytolytie in severM v e r t e b r a t e cell systems (15).…”

Section: Infection Of Cultured a R T H R O P O D Cells Resulted In A mentioning

confidence: 99%

“…Mainly used so far for this purpose are cells from mosquitoes which are natural vectors of the viruses concerned. However, several reports provide evidence that, arboviruses are less specific in their ability to infect and multiply in arthropod cell lines than in vector hosts (9). In this study, a PhIebovirus phlebotomus-associated, Toscana virus, was adapted to grow in a mosquito cell line (AP-61) derived from Aedes pseudoscutellaris.…”

Section: Diseussionmentioning

confidence: 97%

Growth of thePhlebovirus Toscana in a mosquito(Aedes pseudoscutellaris) cell line (AP-61): Establishment of a persistent infection

Nicoletti

Verani

1985

Archives of Virology

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Toscana Virus, a sandfly-associated Phlebovirus, was adapted to grow in cultured Aedes pseudoscutellaris (AP-61) mosquito cell line. No evidence of virus growth was seen after primary infection of cell monolayers under maintenance conditions. On the contrary, persistent infections were established by subculturing infected cultures. Cytopathic effect was never observed. Significant titres of virus (10(3)-10(5) PFU/ml), as assayed in Vero cells at 37 degrees C, were released from persistent infected cells after several subcultures at 29 degrees C over a period of six months. The percentage of virus-producing cells in the persistently infected cultures varied from 0.003 to to 0.017 per cent, whereas from 10 to 50 per cent of cells were shown to retain viral antigens by immunofluorescence. The virus released from persistently infected cultures did not show changes in both plaque size and temperature sensitivity from the parental virus. The virus released from persistently infected cultures multiplied in AP-61 cell monolayers reaching relatively high titres (10(4) PFU/ml).

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Replication of Arboviruses in Arthropod in Vitro Systems: An Overview

Cited by 15 publications

References 63 publications

Differences in fusogenicity and mouse neurovirulence of Japanese encephalitis viruses

Differences in fusogenicity and mouse neurovirulence of Japanese encephalitis viruses

Nairovirus RNA Sequences Expressed by a Semliki Forest Virus Replicon Induce RNA Interference in Tick Cells

Growth of thePhlebovirus Toscana in a mosquito(Aedes pseudoscutellaris) cell line (AP-61): Establishment of a persistent infection

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