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HIV-1 vs HIV-2

RYBICKI, ED ED at molbiol.uct.ac.za
Fri Mar 17 03:37:02 EST 1995

> To:            virology at net.bio.net
> From:          "Patrick O'Neil" <patrick at corona>

Patrick: your "reply-to" is incorrect again!

> Subject:       Re: HIV-1 vs HIV-2
> On 16 Mar 1995 bhjelle at unm.edu wrote:
> > 
> > For viruses, as opposed to certain parasites, there is quite
> > a bit of support for the notion of adaptation toward low
> > pathogenicity for the native host, while having significant
> > pathogenicity for non-native hosts.ri. 
> > 
> Not necessarily.  The flu pandemic of 1918 is a nice case in which 
> previously standard flu strain in the United States quickly 
evolved into a
> major killer in the trenches of late World War I.  The flu is 
> transmissible as it is but get a handful of sick soldiers in a 

Now I am not sure it was as simple as that: I remember 
hearing/reading that the "Spanish Flu" was as nasty as it was partly 
because it was allied in many cases with a staph, which provided the 
extracellular protease needed to cleave the 'flu virus 
haemagglutinin in lung tissues (where the protease that normally 
does the job in upper respiratory epithelium does not occur).  
Anyone else hear about that?

> Change the selective pressures to those that allow rapid 
> from host to host and, no matter how long a virus has been 
enjoying a 
> host's hospitality, the more virulent forms will begin to 

Interesting thing about my pet organism (says he, wrenching the 
conversation around to things he knows more about) - maize streak 
virus, an obligately leafhopper-transmitted pathogen of maize that 
makes Ebola look mild (for plants...!) - is that the only disease 
you really see in maize (obviously not the natural host, it was 
imported) is the severe one: mild strains of the virus cause 
transient symptoms, and multiply to far lower concentrations, and 
are therefore far less easily transmitted from infected plants.  YET 
it appears that variation early in an infestation of a maize field 
is far higher, as the virus(es) come in from the grasses via the 
hoppers.  So the host is selcting the more vicious strains (by 
allowing them to multiply best) for onward transmission, once the 
virus has got into the field: hoppers are targetted to sick plants 
because of their colour, and the fact they are "sweeter" and the 
more vicious virus(es) are the ones causing the best and 
longest lasting symptoms.

Not altogether an apposite comparison with HIV(s), but: is it not 
quite possible that in the natural setting, many people are 
inapparently infected with simian lentiviruses and get over them 
quickly?  And that what we see as AIDS-causing viruses are those 
which - as pointed out above by Patrick - have taken advantage of 
changes in selective pressures, and most notably the possibility of 
rapid transmission?

 | Ed Rybicki, PhD          |  (ed at molbiol.uct.ac.za)  |
 | Dept Microbiology        | University of Cape Town  |    
 | Private Bag, Rondebosch  |   7700, South Africa     |          
 | fax: xx27-21-650 4023    |  tel: xx27-21-650 3265   |  
 |       URL: http://www.uct.ac.za/microbiology        |

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