microRNAHerpesviruses are unusual1 in their ability to establish a long-term latent infection in their hosts.  Another unusual2 trait is that herpesviruses apparently all have genes that block MHC class I recognition by cytotoxic T lymphocytes.  (I suspect that we will also find that evasion of NK cells is also universal among herpesviruses, but that’s still a new and growing field.)  The other virus families that are known to evade MHC class I are human adenoviruses, which now turn out to establish true latency;3 HIV (which also has a true latent stage, though I don’t know if it’s relevant here); a handful of poxviruses, which as far as I know don’t do much in terms of latency; and some papillomaviruses4 which I don’t think have a real latent stage.

I’ve noted previously that these two unusual characteristics of herpesviruses may be linked, in that perhaps the herpesvirus MHC class I immune evasion is important for establishing latency.  A review in Nature5 points out that herpesviruses are also unusual in that they tend to have a lot of micro-RNAs, and suggests a similar concept: That herpesviruses use miRNAs to evade the immune system and this is related to their ability to maintain a latent infection.

It seems possible that the presence of miRNAs in herpesviruses is associated with the characteristic ability of herpesviruses to establish long-term latent infections. Avoiding the host immune response is particularly important during latent infection, and viral miRNAs not only have the advantage of not being recognized by the host immune system but also might be an ideal tool for attenuating immune responses by downregulating the expression of key cellular genes. 5


  1. Though not quite unique[]
  2. Though still not quite unique[]
  3. Latent species C adenoviruses in human tonsil tissues. C. T. Garnett, G. Talekar, J. A. Mahr, W. Huang, Y. Zhang, D. A. Ornelles, and L. R. Gooding. J. Virol. doi:10.1128/JVI.02392-08 []
  4. High-risk human papillomavirus E7 expression reduces cell-surface MHC class I molecules and increases susceptibility to natural killer cells. Bottley G, Watherston OG, Hiew YL, Norrild B, Cook GP, Blair GE. Oncogene. 2008 Mar 13;27(12):1794-9.[]
  5. Bryan R. Cullen (2009). Viral and cellular messenger RNA targets of viral microRNAs Nature, 457 (7228), 421-425 DOI: 10.1038/nature07757[][]