Comments on: Virus neutralization by antibodies

By: Should we fear avian H5N1 influenza?

Should we fear avian H5N1 influenza? — Sat, 07 Jan 2012 22:05:15 +0000

[...] against several avian influenza viruses, including H5N1, by hemagglutination-inhibition and neutralization assays. The results indicate that 73 participants (9.1%) had antibody titers against one of two [...]

By: Jess

Jess — Thu, 22 Sep 2011 15:54:00 +0000

Loving the explanation, really helped me out with my homework

By: Jess

Jess — Thu, 22 Sep 2011 15:54:00 +0000

Loving the explanation, really helped me out with my homework

By: Poliovirus with a twelve year incubation period

Poliovirus with a twelve year incubation period — Fri, 29 Jul 2011 17:28:07 +0000

[...] (CVI) in 1991. Patients with this disease lack B lymphocytes and therefore cannot produce antibodies that help control microbial infections. For example, individuals with CVI often develop chronic [...]

By: Ashish Solanki

Ashish Solanki — Fri, 15 Jul 2011 06:14:00 +0000

Really good explanation

By: Brairtoss87

Brairtoss87 — Fri, 20 May 2011 01:08:00 +0000

Thanks for posting this. i really enjoyed reading this.

By: Good

Good — Sun, 03 Apr 2011 06:44:00 +0000

Thanks a lot for a very good explanation.

By: Adeline Wohlhuter

Adeline Wohlhuter — Mon, 07 Feb 2011 21:55:00 +0000

Hi Professor Racaniello,
Many thanks for your fascinating blog and for posting some of your lectures online.
I am currently learning about the dengue virus, and dengue heamorrhagic fever in particular. I had a few questions for you: Structurally and mechanistically (how it binds to a virus), what are the differences between a non-neutralizing and a neutralizing antibody? Also, is it possible to trigger the synthesis of neutralizing versus non-neutralizing antibodies by B cells? In the adaptive immune response, what will determine whether the antibodies produced are neutralizing or not? Or is this “neutralizing” capacity of the antibodies occurring at random during antibody production depending on the epitopes targeted?
I thank you in advance for taking the time to answer.

By: Dna3173

Dna3173 — Fri, 24 Dec 2010 11:30:00 +0000

I do have my chickenpox vaccine, is there any adverse effects if you have contact with a person with chicken pox?

By: Am889182

Am889182 — Mon, 13 Dec 2010 22:14:00 +0000

what purpose do non-neutralizing antibodies serve? what class of antibodies are these?

By: Pedro_pale

Pedro_pale — Sat, 07 Aug 2010 05:43:16 +0000

WHAT KIND NEUTRALIZING ANTIBODIES ARE INVOLVED AFTER AN INFECTION BY FLAVIVIRUSES SUCH AS DENGUE, SAINT LOUIS,OR ROCIO VIRUS ? THANKS

By: medyum

medyum — Fri, 30 Jul 2010 15:02:42 +0000

Haha, that's a vivid explanation image.

By: Uninstall Program

Uninstall Program — Thu, 17 Jun 2010 13:49:25 +0000

Haha, that's a vivid explanation image.

By: Natural antibody protects against viral infection

Natural antibody protects against viral infection — Fri, 14 May 2010 13:43:07 +0000

[...] Antibodies produced by infection with a virus, or after immunization with viral vaccines, are effective at preventing viral disease. However humans and higher primates contain “natural antibodies” which are present in serum before viral infection. Natural antibodies can activate the classical complement pathway leading to lysis of enveloped virus particles long before the adaptive immune response is activated. [...]

By: profvrr

profvrr — Sun, 25 Apr 2010 08:09:37 +0000

Multivalent doesn't help, because the virus drifts each year
antigenically, and the direction can't be predicted. What is needed is
a cross-protective vaccine, which has not been developed. There have
been some inroads and you can read about them on this blog, for
example: http://www.virology.ws/2009/02/25/influenza-vac....

By: fbedoya

fbedoya — Sun, 25 Apr 2010 06:24:14 +0000

Dear Prof. Racaniello,
Thank you very much for your responses (very accurate and to the point). I am an influenza fan. I have also been doing some research on influenza for the past year, and I become more and more interested on the topic as I learn more about it. I read an article on Science this week about cross-protection between neutralizing Abs against 1918 HA and 2009 HA. I have always wondered if a 'multi-valent' vaccine (including multiple HAs, more than 3) would be more efficacious to generate a more protective response against new viral HAs. Has any lab tried this before? Is this a real possibility?
Many thanks.

By: profvrr

profvrr — Sun, 25 Apr 2010 01:09:37 +0000

By: fbedoya

fbedoya — Sat, 24 Apr 2010 23:24:14 +0000

By: profvrr

profvrr — Tue, 16 Mar 2010 14:12:59 +0000

It's an interesting question that has been studied theoretically and
experimentally. Intuitively it would seem that occupation of all
attachment sites with antibodies would be needed to block attachment.
However, for influenza virus, as few as 1-2 antibodies per virion have
been shown to be sufficient to neutralize influenza virus. The
assumption is that few antibodies can cause conformational changes in
the envelope which blocks attachment. Alternatively, such antibodies
might act catalytically and block fusion.

By: Leticia

Leticia — Tue, 16 Mar 2010 13:12:08 +0000

Is it possible to know how many antibodies are needed to neutralize a virus?
Thanks

By: mdubuque

mdubuque — Fri, 07 Aug 2009 17:26:20 +0000

Thanks for the clarification on "live, attenuated virus" that I, as an informed lay person, have encountered on several occasions. That phrasing had led me to wonder if there was a controversy about whether viruses were alive. Clearly there is no controversy.

Interesting about viruses possibly taking advantage of infectivity enhancing characteristics of selected antibodies. I often find the most fascinating stories in evolutionary biologies to be those discussing the co-evolution of two or more symbiotic organisms, as Lynn Margulis (originator of the notion that the distinct DNA in mitochondria is evidence of cells being a product of co-evolution) as she describes in "Acquiring Genomes: A Theory of the Origin of Species".

http://www.amazon.com/Acquiring-Genomes-Theory-...

It would seem to be an interesting pathway for viral evolution. Sets of viruses may be evolving to directly enter the cell, while other sets may be evolving towards getting their "foot in the door" via alternate pathways such as this. Fascinating stuff, to me at least!

By: profvrr

profvrr — Wed, 05 Aug 2009 20:19:37 +0000

This is a very good question – but the answer is long and deserves a
post of its own. CTLs are generally involved in clearing, not
preventing infections. But the kinds of T cells that are produced do
vary among different types of vaccines. I promise I'll cover this in a
subsequent post. As for escape – T cell epitopes are also short and
known to change so as to avoid CTL killling.

By: profvrr

profvrr — Wed, 05 Aug 2009 20:17:31 +0000

I didn't answer the last part of your question – do viruses 'use' this
method of entering cells. We think so, but we are not sure. Dengue
virus may be one that enters cells via antibody-mediated uptake.

By: profvrr

profvrr — Wed, 05 Aug 2009 20:17:27 +0000

Clearly the statement 'live, attenuated vaccine' is incorrect.
Unfortunately I am guilty of using that phrase for years, but it's
wrong. It's ensconced in the literature and will be difficult to
purge. It should read 'infectious, attenuated vaccine'. Recently I
read an article entitled 'Live Marburg virus isolated from bats' and I
made a point to tell the writer that it should be 'infectious'. As for
antibodies enhancing infectivity on occasion - not all antibodies made
against a virion are able to block infectivity. The antibodies may
bind to the virus, but they do not inhibit infection. Such antibodies
can lead to enhancement of infectivity, because the antibody - via the
Fc portion - can bind to receptors on cells not normally infected by
the virus. The virus-antibody complex is taken up into cells, and
infection proceeds.

By: mdubuque

mdubuque — Sat, 01 Aug 2009 20:58:42 +0000

I'm puzzled trying to reconcile two statements.

1. Viruses cannot be killed because they were never alive, and
2. The Sabin polio vaccine is a "live, attenuated vaccine".

Also, I'm puzzled by this ostensibly counterproductive relationship (on occasion) between non-neutralizing antibodies and viruses when you state that occasionally these particular antibodies may actually ENHANCE infectivity.

Does this mean that some of these non-neutralizing antibodies have the characteristics of "bad actors"?

Do virus populations ever take advantage of this occasional infectivity quotient amplification by such non-neutralizing antibodies?

By: albatross

albatross — Sat, 25 Jul 2009 05:01:58 +0000

Is there a good understanding of what different parts of the immune response the inactivated vs. live attenuated vaccines trigger? It seems like the attenuated virus should produce a CTL response (so I end up with a fair population of CTLs ready to clear infected cells when they start showing flu peptides on their MHC1 molecules). Is that right, or does whatever is done to attenuate the virus keep it from producing that kind of response?

I'm wondering if this might become important, if most people get the inactivated vaccine. That should cause some selection of the flu virus to mutate the bits that stick out of the envelope of the virus (the H and the N), so that the antibodies can't stick to it. But the CTL response (as well as the Th1 response, I think) might not be selected against so strongly.