Thursday, September 17, 2009

Ninja viruses, a (free) radical take on aging and more in my picks of the week from RB

Another week has gone by and some very interesting molbio blog posts have been aggregated into Every week [see my opening post on the matter], I'll select some blog posts I consider particularly interesting in the field of molecular biology [see here to get a sense of the criteria that will be used], briefly describe them and list them here for you to check out.

Note that I'm only taking into consideration the blog posts aggregated under "Biology".

This week, three blog posts made the list:

1. For them to be “successful”, viruses must be able to cope with the host’s immune system: they must evade defense responses. Viruses possess a series of “immune evasion genes” that help them do just that. Influenza, as expected, also has its own set of immune evasion genes, the most important one being the NS1 gene, which blocks the interferon pathway. We know NS1 is important for the virus, as recombinant influenza viruses lacking the NS1 protein are incapable of replicating efficiently in immunocompetent animals. We also know, however, that interferon is important in the antiviral response against influenza, so:
(…) there’s a bit of a paradox here. We know that NS1, the interferon blocker, is important to influenza virus. But we also know that interferon is very important in controlling influenza virus infections. For example, mice that can’t respond to interferons are much more susceptible to infection with avian influenza. So if NS1 works by blocking interferon, why does interferon still protect?
Ian York at Mystery Rays from Outer Space, discusses a recent article1 shedding light on this apparent contradiction. It looks like NS1 helps to keep influenza in "a time-limited 'stealth phase' during which the replicating influenza virus remains undetected, thus preventing the immediate initiation of innate and adaptive immunity". Apparently, it may all be about timing.

2. The widely known “mitochondrial free radical theory of aging”, states that “the macromolecular damage that results from the production of toxic reactive oxygen species (ROS) during cellular respiration is the cause of aging”2

Chris Patil at Ouroboros sets the frame for an interesting discussion: is this theory still valid? Chris comments on a recent review arguing that it should be to put to rest, while also directing us to some of his previous (and fascinating) posts on the subject, to exemplify that there’s still no final say on the matter:
I doubt very much that this article will put a permanent end to the controversy. Data reported fairly recently have breathed new life into oxidative theories in general and the MFRTA in particular.

3) Finally, I'd also like to highlight a nice post from our very own Francisco Barriga, who discusses a recent article3 from Bob Weinberg's lab, where a high-throughput screen to identify chemical agents that could selectively target cancer stem cells, is presented.

Despite the excitement such a study can generate, Pancho calls for caution:
Only time will tell if the CSC hypothesis holds true for all or certain types of tumors and whether if this has any clinical relevance.
That's it for this week. Stay tuned for more MolBio Research Highlights!

Some of the articles discussed in this week's selected posts:
Moltedo, B., Lopez, C., Pazos, M., Becker, M., Hermesh, T., & Moran, T. (2009). Cutting Edge: Stealth Influenza Virus Replication Precedes the Initiation of Adaptive Immunity The Journal of Immunology, 183 (6), 3569-3573 DOI: 10.4049/jimmunol.0900091

Lapointe, J., & Hekimi, S. (2009). When a theory of aging ages badly Cellular and Molecular Life Sciences DOI: 10.1007/s00018-009-0138-8

Gupta, P., Onder, T., Jiang, G., Tao, K., Kuperwasser, C., Weinberg, R., & Lander, E. (2009). Identification of Selective Inhibitors of Cancer Stem Cells by High-Throughput Screening Cell, 138 (4), 645-659 DOI: 10.1016/j.cell.2009.06.034

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