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TWiV 124 Letters

Norm writes:

First, I love your podcasts.

You guys are constantly grousing about the lack of research funding.

I was curious.

NIH, funding has risen every year since 2000, from $17B to the current $31B (supports 325,000 researchers)

NSF funding has risen every year since 2000, from $2.5B to $5.5B

I assume money is also available from Corporations, Charities, Foundations, State Governments, Foreign governments, Department of Defense, CDC, FDA, Universities, etc.

Looks to me like we are spending lots of money on research.

I wonder...

Is it possible that we are not spending money on the "right" things because politics and bureaucracy push the money to the "wrong" things?

My local government spends lots of money, but strangely never seems to be able to fix potholes. Some people say we need to give the government more money so they can fix the potholes, but when get more money, the potholes stay unfixed. Strange that.

I am suspicious that you could double the funding of NIH and research you advocate would still not get funded and you would still be complaining about too little money for research.

As a last thought, it seems to me that the cost of research should be going down, after all much of modern research equipment and services are computer based and these should get cheaper and more powerful every year.

Am I missing something?


Lynn Enquist writes:

I enjoyed hearing you discuss our recent paper on some basic virology using colorful herpesviruses. I have some answers to questions you raised about the phenomenon of limited viral genome expression and replication.

First, the FACs sorting experiment says that the viral genomes that are being expressed in the cell are the same ones that are replicated and packaged. Expression, replication, packaging are all linked! You don’t have a pool of genomes all expressing things and a subset get replicated. Or a random pool of genomes replicating and expressing with a subset being packaged. Rather, a few genomes are chosen early to be transcribed, replicated, and packaged in to virions (that go on to infect the next cell).

Second, Oren has shown that the effect is not due to the promoter used. He did a beautiful set of experiments where the PRV VP26 capsid protein was fused to each of three different fluorescent proteins and these hybrid genes replaced the normal VP26 gene. These hybrid genes are transcribed from the VP26 promoter – which is a PRV promoter expressed only after DNA begins to replicate. Cells infected with mixtures of these viruses reproduce the same phenomenon as we reported in the paper. They also provide more data since these fusion proteins assemble into capsids in the nucleus. The dots of colors in each nucleus are all the same color verifying again that only a few genomes are chosen to be expressed and replicated. Amazing, I think (and very colorful too, for Rich’s benefit).

Oren has infected primary neurons, primary fibroblasts, and other cell lines with the colorful herpesviruses we have on hand. All cells show the same restriction of color as we reported.

Lynn Enquist
Professor, Princeton University


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