Comments on: HERVs: zombie target practice for immunity

By: Cotch dot net

Cotch dot net — Sun, 18 May 2008 17:07:53 +0000

The Molecular and Cell Biology Carnival #2…

Welcome to the second Carnival of Molecular and Cell Biology! …

By: Mystery Rays from Outer Space - Meddling with things mankind is not meant to understand. Also, pictures of my kids » More HERVs

Thu, 08 May 2008 03:10:46 +0000

[...] HERVs: zombie target practice for immunity [...]

By: iayork

iayork — Mon, 05 May 2008 17:46:21 +0000

Do you think this would really work in general? I am sure you know that in bone marrow transplantation, graft-versus-host disease has an important role in clearing the tumorâ€¦

It seems pretty clear this isn’t a universal solution, because only a fraction of tumours upregulate any kind of HERV proteins. A reasonable fraction upregulate the HERV-K groups, but since normal tissues also have some HERV-K expression also, this is probably a suboptimal target. The HERV-E are a more exciting target, but they also seem to be present only in a smallish subset of tumours; perhaps not much more than the clear cell variant of kidney tumour, or perhaps a few more than that.

Still, it is an intriguing idea, and if there is a solution to the potential autoimmunity issue the HERVs might make useful targets for a fair number of tumours types.

I was wondering whether you would be interesting in hosting, or submitting this article to, the Molecular and Cell biology blog carnival.

Thanks for the reminder. I will submit something to the carnival, maybe this one.

By: iayork

iayork — Fri, 02 May 2008 01:17:03 +0000

Although I haven’t followed it closely, I’ve been skeptical about the HERV/MS connection (as I mention in the post). The Antony et al paper you mention has made me less skeptical, but I’m still far from convinced.

In particular, epidemiology hasn’t consistently supported a connection (for example, Ruprecht K, Gronen F, Sauter M, Best B, Rieckmann P, Mueller-Lantzsch N (2008) Lack of immune responses against multiple sclerosis-associated retrovirus/human endogenous retrovirus W in patients with multiple sclerosis. J Neurovirol 14:143â€“151.) Without epidemiological support the proposed biological mechanisms are less exciting. (That said, I’m aware that the epidemiology in this situation is particularly tricky, and that there is some epidemiological support out there.)

In any case, the MSRVs are from a W-group HERV, while most interest in HERVs as tumor antigens has focused on HERV-K and (here) HERK-E. As I mentioned, the HERV-E group has very restricted tissue expression, making it a potentially more specific target even than the HERV-K, where you’re looking for relative differences in expression rather than an on/off situation.

By: CAE

CAE — Fri, 02 May 2008 00:53:17 +0000

Of course the problem with targeting something as ubiquitous as ERVs is that you risk some kind of autoimmune reaction. There is increasing evidence that ERV reactivation is behind diseases like MS, for instance.

By: steppen wolf

steppen wolf — Thu, 01 May 2008 23:35:59 +0000

I love the post – and the topic. Do you think this would really work in general? I am sure you know that in bone marrow transplantation, graft-versus-host disease has an important role in clearing the tumor…

I was wondering whether you would be interesting in hosting, or submitting this article to, the Molecular and Cell biology blog carnival.

If you are…drop me a line!