Re: [asa] Medicine and Evolution

I think you're overreacting Rich. He expressly states his special
definition of "Darwinism": "Darwinism, *understood as the view that "chance
and necessity" explains all biological complexity*, plays no role." You
might critique him on this definition game -- obviously, duh, the study of
disease resistance isn't an effort to "explain all biological complexity" --
but I don't see any suggestion here that we should stop studying who viruses
mutate.

On Fri, May 30, 2008 at 11:01 AM, Rich Blinne <rich.blinne@gmail.com> wrote:

> On Fri, May 30, 2008 at 7:36 AM, David Opderbeck <dopderbeck@gmail.com>
> wrote:
>
>
>
>> C'mon Rich. You know that when someone like Stein says "evolution" they
>> don't mean viral resistance to drugs. There's a huge definitional problem
>> here with the term "evolution," but let's not fall for the schtick that ID
>> advocates don't care about poor people with AIDS. It's as lame as the
>> schtick that evolutionary biologists are all cousins of Hitler.
>>
>
> I'm not interested in Ben Stein's views because the interviews of him show
> him to be an amazingly unreflective and sloppy thinker. He just parrots what
> others tell him. Egnor's views, on the other hand, are what I care about.
> Here's what Egnor said about drug resistance.
>
> Preventing the emergence of resistant strains of bacteria is important
>> work, but the insight that Darwinism brings to the problem – the unkilled
>> ones eventually outnumber the killed ones – is of no help. We can figure
>> that out ourselves. The tough work on preventing the emergence of resistant
>> bacteria is done by microbiologists, epidemiologists, molecular geneticists,
>> pharmacologists, and physicians who are infectious disease specialists.
>> Darwinism, understood as the view that "chance and necessity" explains all
>> biological complexity, plays no role.
>
>
> But the paper put it this way
>
> HIV-1 transmission in humans results most commonly from virus exposure at
>> mucosal surfaces (1). For practical reasons, it has been impossible to
>> identify and characterize by direct analytical methods HIV-1 at or near the
>> moment of transmission, yet it is this virus that antibody or cell-based
>> vaccines must interdict. An important step in achieving a molecular
>> understanding of HIV-1 transmission and potentially in the development of an
>> effective HIV/AIDS vaccine is an accurate and precise description of the
>> transmitted or early founder virus (or viruses) and sequences evolving from
>> them during the critical period leading to productive clinical infection.
>
>
>
>
>> The objective of the present study was to develop and implement an
>> experimental strategy that would enable us to identify unambiguously the
>> transmitted or early founder env genes of viruses responsible for
>> establishing productive HIV-1 infection, to track their evolution in the
>> critical period between transmission, peak viremia and seroconversion, and
>> to evaluate their phenotypic properties. Essential to this strategy were two
>> findings. First was the demonstration by Leigh Brown and coworkers (15),
>> Mullins and coworkers (19), Coffin and coworkers (16), and Hahn and
>> coworkers (17) that single genome amplification (SGA) of HIV-1 plasma vRNA
>> followed by direct sequencing of uncloned amplicon DNA precludes Taq-induced
>> nucleotide misincorporation and recombination in finished sequences. Second
>> were the observations by Ho and coworkers (21, 22) and Shaw and coworkers
>> (23, 24) that, because of the extremely short in vivo lifespan of plasma
>> virus and of productively infected cells (t1/2 < 1 day), analysis of plasma
>> vRNA could provide a uniquely informative view of HIV-1 replication dynamics
>> and evolution. Thus, we hypothesized that an SGA-based analysis of plasma
>> vRNA obtained from acutely infected individuals in the earliest stages of
>> infection, and evaluated within the context of a model of random viral
>> evolution, would allow us to infer the nucleotide sequences of env genes of
>> viruses responsible for establishing productive clinical infection weeks
>> earlier.
>>
>
> So, if you take evolution off the table like Egnor does, you don't make
> progress on an HIV/AIDS vaccine. Furthermore, encouraging the next
> generation of doctors to the same is unconscionable. I have no doubts that
> Egnor has compassion for the victims of AIDS but for Ben Stein to imply that
> our motivation is also not marked by compassion simply adds insult to
> injuryl. Note that nowhere did I impute motives like Ben Stein did of mine.
> Rather, my own view is -- to borrow a legal concept -- Egnor is incredibly
> negligent and completely clueless. Egnor stuck his nose into an essay
> contest for the next generation of doctors and biologists and in effect will
> be presenting future studies like above. This is why the innocently sounding
> phrase "teach the controversy" is not so innocent.
>
> Rich Blinne
> Member ASA
>
>
>

-- 
David W. Opderbeck
Associate Professor of Law
Seton Hall University Law School
Gibbons Institute of Law, Science & Technology
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