>*But what if herpes can cross
>between an axon/dendrite and another
>cell body? If this is
>true I can see some
>other internal organs becoming infected
>with HSV becaue it can
>take cutoff to other highways
>instead of changing routes in
>the center of town.
Understaning *how* the virus spreads is interesting. However, it does happen frequently.
>Sometimes GVAs synapse on neurons going
>to the brain. Does that
>lead to herpes menigitis and
>encephalitis? Does that mean herpes
>inadvertently took the "wrong path"
>. (It gets no reproductive
>advantage from heading up there
>or to any other organ.)
While we can rationalize the advantages of one path over another, it's quite possible that HSV has been successful even though it lacked this insight. Meaning, it might have evolved by spreading in multiple directions.>
>Does the virus realise this and
>just doesn't replicate in most
>circumstances which is why we
>don't see more herpes menengitis?
Howl: you keep implying the virus actually *thinks.* Meningitis is quite common -- about 30% of women and 10% of men get meningitis during a primary epsiode. HSV-2 is also the priamry cause of recurrent meningitis (Mollart's meningitis). If you look at autopsy reports, it really is quite invansive.
As an example...
J Pathol 2002 Jul;197(3):395-402 Related Articles, Links
Herpesviruses in brain and Alzheimer's disease.
Lin WR, Wozniak MA, Cooper RJ, Wilcock GK, Itzhaki RF.
Department of Optometry and Neuroscience, UMIST, Manchester, UK.
It has been established, using polymerase chain reaction (PCR), that herpes simplex virus type 1 (HSV1) is present in a high proportion of brains of elderly normal subjects and Alzheimer's disease (AD) patients. It was subsequently discovered that the virus confers a strong risk of AD when in brain of carriers of the type 4 allele of the apolipoprotein E gene (apoE-epsilon4). This study has now sought, using PCR, the presence of three other herpesviruses in brain: human herpesvirus 6 (HHV6)-types A and B, herpes simplex virus type 2 (HSV2) and cytomegalovirus (CMV). HHV6 is present in a much higher proportion of the AD than of age-matched normal brains (70% vs. 40%, p=0.003) and there is extensive overlap with the presence of HSV1 in AD brains, but HHV6, unlike HSV1, is not directly associated in AD with apoE-epsilon4. In 59% of the AD patients' brains harbouring HHV6, type B is present while 38% harbour both type A and type B, and 3% type A. HSV2 is present at relatively low frequency in brains of both AD patients and normals (13% and 20%), and CMV at rather higher frequencies in the two groups (36% and 35%); in neither case is the difference between the groups statistically significant. It is suggested that the striking difference in the proportion of elderly brains harbouring HSV1 and HSV2 might reflect the lower proportion of people infected with the latter, or the difference in susceptibility of the frontotemporal regions to the two viruses. In the case of HHV6, it is not possible to exclude its presence as an opportunist, but alternatively, it might enhance the damage caused by HSV1 and apoE-epsilon4 in AD; in some viral diseases it is associated with characteristic brain lesions and it also augments the damage caused by certain viruses in cell culture and in animals. Copyright 2002 John Wiley & Sons, Ltd.
Keep in mind the servoprevalence of HSV-2 and the age of people with AD and matched controls (this is a UK study) -- quite invasive.
>Or is it that the body
>is better at detecting HSV
>and mounting a response against
>herpes when it is outside
>its usual haunts within the
>nervous system. The virus is
>killed off when it starts
>to take the wrong path?
The virus appears to be successful regardless of its path.
>Or is it that the virus
>can't travel that far b/c
>of the physical barriers the
Obviously it does travel and well.