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Interferon production and signaling pathways are antagonized during henipavirus infection of fruit bat cell lines.

Virtue ER, Marsh GA, Baker ML, Wang LF - PLoS ONE (2011)

Bottom Line: Henipaviruses have been observed both naturally and experimentally to cause serious and often fatal disease in many different mammal species, including humans.We report that henipavirus infection does not result in the induction of interferon expression, and the viruses also inhibit interferon signaling.We also confirm that the interferon production and signaling block in bat cells is not due to differing viral protein expression levels between human and bat hosts.

View Article: PubMed Central - PubMed

Affiliation: Australian Animal Health Laboratory, CSIRO Livestock Industries, Geelong, Australia.

ABSTRACT
Bats are natural reservoirs for a spectrum of infectious zoonotic diseases including the recently emerged henipaviruses (Hendra and Nipah viruses). Henipaviruses have been observed both naturally and experimentally to cause serious and often fatal disease in many different mammal species, including humans. Interestingly, infection of the flying fox with henipaviruses occurs in the absence of clinical disease. The extreme variation in the disease pattern between humans and bats has led to an investigation into the effects of henipavirus infection on the innate immune response in bat cell lines. We report that henipavirus infection does not result in the induction of interferon expression, and the viruses also inhibit interferon signaling. We also confirm that the interferon production and signaling block in bat cells is not due to differing viral protein expression levels between human and bat hosts. This information, in addition to the known lack of clinical signs in bats following henipavirus infection, suggests that bats control henipavirus infection by an as yet unidentified mechanism, not via the interferon response. This is the first report of henipavirus infection in bat cells specifically investigating aspects of the innate immune system.

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Related in: MedlinePlus

Cell type-independent antagonism of the interferon signaling pathway in bat cells.(A) PaFe, PaFeT, PaKi and PaLuT02 cells were infected with HeV at a high MOI for 24 h pi, followed by treatment with Universal Interferon (1000 U) for 3 h. Real-time PCR was then performed for ISG54 and ISG56. N = 2 with error bars indicating SEM. (B) Immunofluorescent staining of duplicate infections were undertaken to determine level of virus infection using HeV P-specific antisera.
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pone-0022488-g003: Cell type-independent antagonism of the interferon signaling pathway in bat cells.(A) PaFe, PaFeT, PaKi and PaLuT02 cells were infected with HeV at a high MOI for 24 h pi, followed by treatment with Universal Interferon (1000 U) for 3 h. Real-time PCR was then performed for ISG54 and ISG56. N = 2 with error bars indicating SEM. (B) Immunofluorescent staining of duplicate infections were undertaken to determine level of virus infection using HeV P-specific antisera.

Mentions: Due to the differences observed following henipavirus infection and interferon signaling in bat cells compared to human cells, the experiment was repeated in several different P. alecto cell lines. Cells were infected with HeV in order to determine whether a block in interferon signaling is universal or unique to the PaLuT02 cells. Primary fetus and kidney cells (PaFe and Paki), and cloned, immortalised fetus and lung cells (PaFeT and PaLuT02) were infected with HeV for 24 h at a high MOI and were treated with Universal Interferon (1000 U) for 3 h prior to harvesting for real time assays (Figure 3a). A percentage block in ISG54 and ISG56 induction was calculated with mock-infected cells being set at 100% for each cell type. In all cell types there was at least a 75–80% reduction in ISG54/56 transcription compared to mock-infected cells (Figure 3a). Immunofluorescent detection of duplicate HeV infected cells confirmed a 75–80% level of infection (Figure 3b).


Interferon production and signaling pathways are antagonized during henipavirus infection of fruit bat cell lines.

Virtue ER, Marsh GA, Baker ML, Wang LF - PLoS ONE (2011)

Cell type-independent antagonism of the interferon signaling pathway in bat cells.(A) PaFe, PaFeT, PaKi and PaLuT02 cells were infected with HeV at a high MOI for 24 h pi, followed by treatment with Universal Interferon (1000 U) for 3 h. Real-time PCR was then performed for ISG54 and ISG56. N = 2 with error bars indicating SEM. (B) Immunofluorescent staining of duplicate infections were undertaken to determine level of virus infection using HeV P-specific antisera.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3139658&req=5

pone-0022488-g003: Cell type-independent antagonism of the interferon signaling pathway in bat cells.(A) PaFe, PaFeT, PaKi and PaLuT02 cells were infected with HeV at a high MOI for 24 h pi, followed by treatment with Universal Interferon (1000 U) for 3 h. Real-time PCR was then performed for ISG54 and ISG56. N = 2 with error bars indicating SEM. (B) Immunofluorescent staining of duplicate infections were undertaken to determine level of virus infection using HeV P-specific antisera.
Mentions: Due to the differences observed following henipavirus infection and interferon signaling in bat cells compared to human cells, the experiment was repeated in several different P. alecto cell lines. Cells were infected with HeV in order to determine whether a block in interferon signaling is universal or unique to the PaLuT02 cells. Primary fetus and kidney cells (PaFe and Paki), and cloned, immortalised fetus and lung cells (PaFeT and PaLuT02) were infected with HeV for 24 h at a high MOI and were treated with Universal Interferon (1000 U) for 3 h prior to harvesting for real time assays (Figure 3a). A percentage block in ISG54 and ISG56 induction was calculated with mock-infected cells being set at 100% for each cell type. In all cell types there was at least a 75–80% reduction in ISG54/56 transcription compared to mock-infected cells (Figure 3a). Immunofluorescent detection of duplicate HeV infected cells confirmed a 75–80% level of infection (Figure 3b).

Bottom Line: Henipaviruses have been observed both naturally and experimentally to cause serious and often fatal disease in many different mammal species, including humans.We report that henipavirus infection does not result in the induction of interferon expression, and the viruses also inhibit interferon signaling.We also confirm that the interferon production and signaling block in bat cells is not due to differing viral protein expression levels between human and bat hosts.

View Article: PubMed Central - PubMed

Affiliation: Australian Animal Health Laboratory, CSIRO Livestock Industries, Geelong, Australia.

ABSTRACT
Bats are natural reservoirs for a spectrum of infectious zoonotic diseases including the recently emerged henipaviruses (Hendra and Nipah viruses). Henipaviruses have been observed both naturally and experimentally to cause serious and often fatal disease in many different mammal species, including humans. Interestingly, infection of the flying fox with henipaviruses occurs in the absence of clinical disease. The extreme variation in the disease pattern between humans and bats has led to an investigation into the effects of henipavirus infection on the innate immune response in bat cell lines. We report that henipavirus infection does not result in the induction of interferon expression, and the viruses also inhibit interferon signaling. We also confirm that the interferon production and signaling block in bat cells is not due to differing viral protein expression levels between human and bat hosts. This information, in addition to the known lack of clinical signs in bats following henipavirus infection, suggests that bats control henipavirus infection by an as yet unidentified mechanism, not via the interferon response. This is the first report of henipavirus infection in bat cells specifically investigating aspects of the innate immune system.

Show MeSH
Related in: MedlinePlus