Field of Science

A bat virus that can't fight your immune system

I have been too busy to go into this in much detail but I'm wondering whether anyone had any ideas as to why this virus (cedar virus - a newly discovered bat RNA virus) appears not to be able to combat the human innate immune system, specifically: HeLa cell secretion of beta interferon in cell culture.

 1) is this real?

2) does a virus have to be able to combat this part of the immune system?

3) why use a human  cell culture to study a bat virus? and finally,

 4) what does this mean for the virus in a bat?

Cedar Virus: A Novel Henipavirus Isolated from Australian Bats


The genus Henipavirus in the family Paramyxoviridae contains two viruses, Hendra virus (HeV) and Nipah virus (NiV) for which pteropid bats act as the main natural reservoir. Each virus also causes serious and commonly lethal infection of people as well as various species of domestic animals, however little is known about the associated mechanisms of pathogenesis. Here, we report the isolation and characterization of a new paramyxovirus from pteropid bats, Cedar virus (CedPV), which shares significant features with the known henipaviruses. The genome size (18,162 nt) and organization of CedPV is very similar to that of HeV and NiV; its nucleocapsid protein displays antigenic cross-reactivity with henipaviruses; and it uses the same receptor molecule (ephrin- B2) for entry during infection. Preliminary challenge studies with CedPV in ferrets and guinea pigs, both susceptible to infection and disease with known henipaviruses, confirmed virus replication and production of neutralizing antibodies although clinical disease was not observed. In this context, it is interesting to note that the major genetic difference between CedPV and HeV or NiV lies within the coding strategy of the P gene, which is known to play an important role in evading the host innate immune system. Unlike HeV, NiV, and almost all known paramyxoviruses, the CedPV P gene lacks both RNA editing and also the coding capacity for the highly conserved V protein. Preliminary study indicated that CedPV infection of human cells induces a more robust IFN-β response than HeV.


  1. Answers:
    1) yes, why not?
    2) it certainly helps
    3) because it was the only one they had around that the virus grew in
    4) very little!

  2. Thanks for your comments Ed

    My point with asking was it real is that I am not sure how they have propagated the virus. A) the growing of the virus could have lacked selection for interferon antagonism (if using veros) and B) they may have generated lots of defective interfering particles in their stocks. Also this virus may have only started out as a single particle in the bat urine. This virus could have been 'unfit' in a bat. What I wanted was them to sequence 'clinical' material from bats to prove that these virus lack IFN antagonism.

    And all your other points I agree with. Sadly it seemed a little rushed. They do have bat cell lines so they mustnt have used them for a reason. And then you've got to ask: why the heck doesn't grow in the cells?

  3. Hi Conner,

    In answer to your question its always of interest to test the ability of viruses to combat the early innate immune response. The other henipaviruses (Nipah and Hendra) encode proteins able to impair the IFN system and they are of bat origin also so it makes sense to test this ability of a new and related virus in a similar manner.

    A more interesting point to me from virus evolutionary standpoint is the finding that the virus shares the same receptor as the henipaviruses yet has a genome structure more similar to respiro- and avulaviruses

    1. Totally agree with your first point - I wasn't commenting on whether the experiments were worthwhile (it's always good to be at least one step ahead of Nature) but I was talking about the relevance of their results. Interesting as they may be.

      While yes this virus appears to use Ephrin-B2 as a receptor for cell-cell spread at least (they didn't do entry studies so I can't comment) I don't agree that it has a genome structure more similar to respiro and avula viruses. It has the typical paramyxovirinae structure (3'-N-P/V-M-F-G-L-5') without additional genes prior to N like RSV and MPV which are both Pneumovirinae. Avulaviruses - as members of the Paramyxovirinae - like NDV edit their V/P ORF to generate multiple products but cedar virus appears not to do this and doesn't even have a V ORF. This virus is clearly a divergent member of the henipaviruses.


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