Topic: Original antigenic sin This might be whats happened in Bb???
treepatrol
Honored Contributor (10K+ posts)
Member # 4117
posted
Original antigenic sin
Original antigenic sin (first described in 1960 by Thomas Francis, Jr. in the article On the Doctrine of Original Antigenic Sin[1], also known as the Hoskins effect[2]) refers to the propensity of the body's immune system to preferentially utilize immunological memory based on a previous infection when a second slightly different version, of that foreign entity (e.g. a virus or bacterium) is encountered.
This leaves the immune system "trapped" by the first response it has made to each antigen, and unable to mount potentially more effective responses during subsequent infections.
The phenomenon of original antigenic sin has been described in relation to influenza virus, dengue fever, human immunodeficiency virus (HIV), and to several other viruses.
It is named by analogy to the theological concept of original sin.
In B cells
During a primary infection, long-lived memory B cells are generated, which remain in the body, and provide protection from subsequent infections.
These memory B cells respond to specific epitopes on the surface of viral proteins in order to produce antigen-specific antibodies, and are able to respond to infection much faster than B cells are able to respond to novel antigens. This effect shortens the amount of time required to clear subsequent infections.
Between primary and secondary infections, or following vaccination, a virus may undergo antigenic drift, in which the viral surface proteins (the epitopes) are altered through natural mutation, allowing the virus to escape the immune system.
When this happens, the altered virus preferentially reactivates previously activated high-affinity memory B cells and spur antibody production. However, the antibodies produced by these B cells generally ineffectively bind to the altered epitopes. In addition, these antibodies inhibit the activation of lower-affinity naive B cells that would be able to make more effective antibodies to the second virus. This leads to a less effective immune response and recurrent infections may take longer to clear.
Original antigenic sin is of particular importance in the application of vaccines. The specificity and the quality of the immune response is often diminished in individuals who are repeatedly immunized (by vaccination or recurrent infections).
However, the impact of antigenic sin on protection has not been well established, and appears to differ with each infectious agent vaccine, geographic location, and age.
In cytotoxic T cells
A similar phenomenon has been described in cytotoxic T cells (CTL).[5] Several groups have attempted to design vaccines for HIV and hepatitis C based on induction of cytotoxic (CTL) responses. The recent finding that CTL may be biased by original antigenic sin, may help to explain the limited effectiveness of these vaccines.
Viruses like HIV are highly variable and undergo mutation frequently, and thus, due to original antigenic sin, HIV infection induced by viruses that express slightly different epitopes (than those in a viral vaccine) would fail to be controlled by the vaccine. In fact, the vaccine might make the infection even worse,by "trapping" the immune response into the first, ineffective, response it made against the virus.
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
Truthfinder
Frequent Contributor (1K+ posts)
Member # 8512
posted
Fascinating, Tree.... I'd never heard of this before.
They talk here of viruses - I wonder if the same is true of bacteria? I don't know why it wouldn't be, bacteria mutate/change, too.
I guess we rely on those NK cells to pick up the slack when there is a new pathogen on the block.
Tracy
-------------------- Tracy .... Prayers for the Lyme Community - every day at 6 p.m. Pacific Time and 9 p.m. Eastern Time � just take a few moments to say a prayer wherever you are�. Posts: 2966 | From Colorado | Registered: Dec 2005
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treepatrol
Honored Contributor (10K+ posts)
Member # 4117
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quote:Originally posted by Truthfinder: Fascinating, Tree.... I'd never heard of this before.
Tracy
I never did either cant believe I never ran into it after all these years searching.
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
treepatrol
Honored Contributor (10K+ posts)
Member # 4117
posted
up
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
"The overall aim of the study is to investigate the role of infection with B. garinii or B. afzelii and simultaneous or sequential infection with B.burgdorferi s.s. on murine immune responses and thereby the severity of murine Lyme arthritis....
"We hypothesise that mixed infections alter murine immune responses and enhance the severity of Lyme arthritis. Possible mechanisms involved are 'immunodominance' and 'original antigenic sin' [Frank 2002; Klenerman 1998]."
I'd like to see this studied beyond arthritis. We know arthritic-sx and neuroinvasive strains of Bb express surface proteins differently (that's why Igenex uses 2 strains).
Is it possible that the reason so many neuro Lyme patients remain ill is that they were initially infected (unknowingly, perhaps) with a milder arthritic strain that primed their immune system, before getting a neuro strain??
Could it be that mild, arthritic (asymptomatic?) strains are more common after all - maybe really common - and that's a key problem for those of us who contract a neuro strain afterwards?
Just thinking out loud. Thanks for posting this.
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