Lupus- Bacterial or Viral?

Question

So I know lupus is neither but is there a way that it is connected?

Answer 1

no....lupus makes your immune system weak so you can get stuff easier but viruses and bacteria dont cause lupus in any way

Answer 2

It's a great question. Systemic Lupus Erythematous (SLE) has no proven microbial cause but in recent years some scientists are trying to show that viruses play a role. What you can find is that some viruses can cause SLE mediated by polyamines. It takes a lot of time and stamina, however, to prove the actual cause and effect relationship between infectious agents and autoimmune disorders like SLE.
At the bottom you can find a weblink to some relevant papers. Also I copy and paste two abstract for you. Good luck


Med Hypotheses. 2004;62(2):237-46.

Calculating the etiology of systemic lupus erythematosus.

Adhami E.

Department of Anesthesiology and Critical Care, College of Medicine, University
of Florida, 945 NW 114th way, Gainesville, FL 32606, USA. [e-mail]

Objective was to clarify the etiology and pathogenesis of systemic lupus
erythematosus (SLE). Drug-induced lupus (DIL) and SLE are both found in humans,
are exacerbated by the same viruses or drugs, and they are both more common in
slow acetylators. Thus, DIL can be used as a model for SLE and the Adhami
equation of DIL can be applied to SLE. Polyamines are the only possible link
between the viral and amine hypotheses of SLE pathogenesis. Based on the Adhami
equation, polyamines can explain the actual annual incidence of SLE in the
general population. Putrescine is a very weak SLE-causing agent, while spermine
and spermidine contribute equally in triggering SLE. The positively charged
polyamines bind to negatively charged internucleosomal DNA and change its
conformation from B (non-immunogenic) to Z (immunogenic). This is the major
contribution of polyamines in triggering SLE. The other effects of polyamines
are only secondary. Apoptosis is a necessary step in SLE pathogenesis, because
it causes the internucleosomal fragmentation of DNA and exposes Z-DNA to the
immune system (due to cell death). The next step is the production of anti-DNA
antibodies, followed by other SLE phenomena. Polyamines not only cause SLE, but
they are also important in sustaining the disease. Other endogenous and
exogenous amines have additive effects with polyamines and may contribute in
exacerbating SLE. When SLE is in the active phase, polyamine levels are higher
as compared to remissions. Fluctuations in polyamine levels due to diet,
metabolic factors, infections, intestinal flora, etc. or the presence of other
amines may explain the course of SLE, characterized by remissions and
exacerbations. Acetylcysteine is a drug that can be completely metabolized to
acetyl groups. As such, this drug is proposed as the ideal acetyl donor for the
acetylation of polyamines and other SLE-triggering compounds. Clinical trials
will be necessary to test the role of acetylcysteine in the etiologic treatment
of SLE. Conclusions: Changes in DNA conformation by polyamines are the first
step in SLE pathogenesis. Many genetic and environmental factors may increase or
decrease the effects or levels of polyamines, causing SLE exacerbations or
remissions. Viruses and other infectious agents may cause SLE by producing
polyamines or by increasing the levels of endogenous polyamines. The major
autoimmune diseases are characterized by remissions and exacerbations and not by
a continuously progressive course, as commonly believed. Consequently, they are
not sustained by internal vicious cycles, but by the initial triggering
agent(s). While the conventional treatment of autoimmune disorders is important
in minimizing tissue damage, the neutralization of their etiology may be
important in curing and preventing autoimmunity.



Autoimmunity. 2005 Nov;38(7):465-72.

Environment and systemic lupus erythematosus: an overview.

Sarzi-Puttini P, Atzeni F, Iaccarino L, Doria A.

Rheumatology Unit, Department of Rheumatology, L Sacco University Hospital,
Milan, Italy. [e-mail]

Systemic lupus erythematosus (SLE) is an autoimmune disease of unknown etiology
that manifests as a pleomorphic systemic disease mainly affecting females. The
variety of autoantibodies found in the serum of patients indicate that SLE is an
autoimmune disease, but the mechanisms leading to the aberrant responses are not
clearly understood although it is thought that a number of genetic and
environmental factors may be involved. Environmental (or non-genetic) exposures
could include infectious agents, chemicals or other compounds capable of
modulating immune responses such as occupational/environmental pollutants or
drugs, and behavioural factors such as smoking and diet. Environmental exposures
may lead to the production of autoreactive T cells and autoantibodies, the
stimulation of pro- and antiinflammatory cytokines, and target end-organ damage,
but are not so convincing as agents causing SLE. Exposure to viruses increases
antibody titres, but these may be the result of polyclonal B cell activation.
The amount and timing of exposure to different environmental factors may play a
significant and complex role in the pathogenesis of SLE and other autoimmune
diseases. A better understanding of the etiopathogenetic mechanism of SLE is
required in order to clarify the multiple interactions between environmental
exposures and genetic factors.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=pubmed_DocSum&db=pubmed&cmd=Display&dopt=pubmed_pubmed&from_uid=14962634