TLR3 & Related Pathways

Both EBV and VZV have very differing life cycles to HSV1 and 2. EBV and VZV both replicate expressing intracellular levels of viral transcripts during clinical quiescence. During quiescence HSV and 2 do  not express viral transcripts, though curiously, HSV 1 and 2 have asymptomatic viral shedding though this does not occur in EBV and VZV.

 

All (except VZV I think) have IL-10 homologues (as does CMV) thought used to prevent the harbouring site being destroyed, though on VZV this perhaps is not useful.

 

Surely his lymphopenia is key.

 

I have a man in mid 50's presented with necrotizing HSV2 (genital) and subsequently has had 3 cutaneous melanoma, and 2 KS. He isn't of the genetic background for KS, and he has neg HIV, but he does have a CD4 count that floats 200-350.

 

I think like in HIV, some people can get CD4 depletion for specific viruses (perhaps under direction of some malfunctioning CD4 memory maintenance).

TLR3 Signalling and Related Pathways

Dear Daman and Stephen,

Thanks for your replies.

 

Daman - I guess there is a reason why patients with TLR deficiency tend to present with HSV rather than other herpesviruses - I must say that you are probably better read up on this than me. But if anyone has a suggestion as to what might be common, it would be welcome. It could be pure coincidence that they are both herpesviruses rather than other opportunistic infections, but it is intriguing...

 

Stephen - He did have EBV NA IgG detected - so I guess it may be reactivation. Unfortunately they did not do any IgM serology at the time (lymphadenopathy occurred back in September) and it may be a bit late now. He had a BM biopsy yesterday and we are waiting for the result.

 

I'll let you know if anything eventuates.

 

Regards,

Catherine

TLR3 Signalling & Related Pathways: From Daman Langguth

Dear Daman and Stephen,

Thanks for your replies.

 

Daman - I guess there is a reason why patients with TLR deficiency tend to present with HSV rather than other herpesviruses - I must say that you are probably better read up on this than me. But if anyone has a suggestion as to what might be common, it would be welcome. It could be pure coincidence that they are both herpesviruses rather than other opportunistic infections, but it is intriguing...

 

Stephen - He did have EBV NA IgG detected - so I guess it may be reactivation. Unfortunately they did not do any IgM serology at the time (lymphadenopathy occurred back in September) and it may be a bit late now. He had a BM biopsy yesterday and we are waiting for the result.

 

I'll let you know if anything eventuates.

 

Regards,

Catherine

TLR3 and Related Pathways: Response from Stephen Adelstein

Catherine,

 

Does he have EBV antibodies?  I would not be dissuaded from considering XLP especially if he does not have anti-EBV antibodies – only a third of patients with XLP have immunodeficiency as far as I understand.  Age is obviously against him, but manifestation of the condition does require exposure to EBV and conceivable (albeit unlikely?) that this had not happened previously…?

 

Would however be concerned about primary marrow problem with secondary VZV and EBV.  Assume rest of haematopoetic cells are normal ? Has he had a bone marrow exam? Etc

 

SA

 

 

 

Stephen Adelstein

Head, Department of Clinical Immunology | Royal Prince Alfred Hospital
Missenden Road, Camperdown, NSW 2050 Australia
Tel 02 9515 7585 | Fax 02 9515 7762 | stephen.adelstein@sydney.edu.au