Polyoma Viruses Cause Lupus

According to the health establishment's ideology of infection-denial, systemic lupus erythematosus (SLE) is a non-infectious, inflammatory, so-called "autoimmune" disorder. According to this delusional mode of thought, some peoples' immune systems are genetically programmed to attack their own bodies. What sets of this attack is a complete mystery, and "treatments" consist mainly of anti-inflammatory, immunosuppressive, and/or cytotoxic drugs.

The symptoms of lupus are diverse. These include a "butterfly" rash across the nose and cheeks, ulcers in the mouth or nose, and hair loss; painful joints; kidney disease; pleurisy, pericarditis and/or peritonitis; vasculitis; abnormalities in the blood cells, including anemia, low white blood cell or platelet count; and nervous system symptoms such as convulsions, psychosis, abnormal sensations, and muscular weakness or lack of coordination.

Commonly used laboratory tests for lupus include the anti-nuclear antibody test (ANA), to determine if there are "autoantibodies" to the cell nuclei; the anti-DNA antibody test; and the anti-Sm antibody test, for antibodies to a protein found in the cell nucleus. According to conventional thinking, these purported antigens are released into the bloodstream due to "aberrant apoptosis" (programmed cell death), of unknown cause, in patients with SLE.

But there are gaping holes in this hypothesis. "Free, naked DNA is not present in the circulation. The existence of DNA/antiDNA complexes is highly questionable and injection of these complexes hardly leads to glomerular localization" in the kidney. Also, "Immunization with DNA in general fails to induce pathogenic anti-dsDNA antibodies" (Autoimmunity against nucleosomes and lupus nephritis. MC Van Bruggen, C Kramers, JH Berden. Ann Med Interne (Paris) 1996;147(7):485-489).

In fact, all of these variety of symptoms are consistent with what has long been known about the effects of human polyomavirus infections. The BK virus and JC virus were both discovered long ago, in 1971. BKV was isolated from a kidney transplant patient (among whom the virus causes tubulonephritis and ureteral stenosis), and JCV from an AIDS patient with progressive multifocal leukoencephalopathy, a demyelinating brain disease. Most of the population worldwide is infected with one or both of these viruses during childhood, and they remain latent in the kidneys (although with occasional reactivations) for life. Reactivations are more common in immunosuppressed persons, such as transplant, cancer chemotherapy, lymphoma, and AIDS patients, but they also occur very frequently during pregnancy (10-37%). And, polyomavirus reactivations have been demonstrated in patients with "noninfectious" diseases including several forms of anemia, nephrotic syndrome, Guillain-Barre syndrome, and in lupus, dating from the latter 1970s. JCV and BKV persistently infect the central nervous system and B lymphocytes, with JCV more neurotropic than BKV, and are also able to persistently infect CD34+ hematopoietic precursor cells, while BKV also infects connective tissue and endothelial cells, causing vasculitis.

A recent study in Norway has directly addressed the role of polyomaviruses BK and JC in SLE. First, in experiments in laboratory mice, they observed that antibodies to DNA and transcription proteins developed only after exposure to polyomavirus T-antigens. Then, over a period of a year, they collected sera monthly, and urine samples every other week, from 20 SLE patients, 6 rheumatoid arthritis patients, and 10 normal controls. None of the normal controls and only one of the six RA patients became PCR-positive for JC or BK polyomavirus, but 16 of the 20 SLE patients did. Their antibody levels to T-antigen and to DNA correlated with the frequency of reactivations. 12 of the 16 were positive for BK virus, 3 for JC, and for one no sequence was obtained. Finally, in a prevalence study, polyoma DNA was found in only one out of 36 RA patients and none of 32 healthy controls, while 43% of SLE patients were positive by PCR. (Experimental expression in mice and spontaneous expression in human SLE of polyomavirus T-antigen. OP Rekvig et al. J Clin Invest 1997 Apr 15;99(8):2045-2054.)

Further evidence that a virus is involved is that T cells did not proliferate in response to histones or nucleosomes, except after this was initiated by T-antigen or T-antigen complexes. (Termination of human T cell tolerance to histones by presentation of histones and polyomavirus T antigen provided that T antigen is complexed with nucleosomes. K Andreassen et al. Arthritis Rheum 1999 Nov;42(11):2449-2460.)

And, cells that are stimulated by certain viral infections synthesize alpha/beta interferons, which induce MxA protein. MxA protein is found in skin lesions with known viral causes, such as chickenpox, herpes zoster, and herpes simplex. It is also found in skin lesions of unknown cause, including lupus erythematosus, lichen planus, Schoenlein-Hennoch's anaphylactoid purpura, and psoriasis. It is not found in non-viral skin infections or certain other skin lesions of unknown cause. (J Fah et al. Expression of MxA protein in inflammatory lesions. J Histochem 1995 Jan;43(1):47-52.)

Why some non-immunosuppressed, non-pregnant people have frequent reactivations while others do not is still unknown. But it could be as simple as that those with frequent recurrences were infected with the virus earlier in life. For example, nearly everyone who has had chickenpox has been latently infected by the varicella-zoster virus, and reactivations, producing shingles, are rare in people under 50 years old. However, shingles occurs much earlier in life in people who had chickenpox before they were two years old. Interestingly, outbreaks of shingles are more frequent in people with lupus than in the general population, so there may be some kind of interaction between these viruses. Unfortunately, there is no drug to treat the polyomaviruses that is like acyclovir for the herpes viruses (although new acyclic nucleoside phosphonates have recently been proved effective in clinical trials). This has not been a priority for the health establishment, which has seen the pathogenic effects in animals while they played with these viruses in the laboratory for nearly 30 years, but denies that they cause disease in people other than AIDS and transplant patients. And they left the human epidemiology to human garbage who ignore infections and the socioeconomic linkages to them, and do surveys of peoples' smoking habits instead.

Polyomaviruses and autoimmunity

Inoculation with BK virus may break immunological tolerance to histone and DNA antigens. T Flaegstad, K Fredriksen, B Dahl, T Traavik, OP Rekvig. Proc Natl Acad Sci U S A 1988 Nov;85(21):8171-8175.

BK virus terminates tolerance to dsDNA and histone antigens in vivo. T Fredriksen, T Traavik, T Flaegstad, OP Rekvig. Immunol Invest 1990 Apr;19(2):133-151. "Antibodies to BK virus structural proteins were detected in all rabbits. Two out of five rabbits produced antibodies to dsDNA, ssDNA, nucleosomes and histones H1 and H3. Even a weak reactivity to H2B was detected in one serum. The autoantibody response was transient as it declined after a few weeks, but it reappeared after a second boost in one of the rabbits."

Antibodies to dsDNA are produced during primary BK virus infection in man, indicating that anti-dsDNA antibodies may be related to virus replication in vivo. K Fredriksen, A Skogsholm, T Flaegstad, T Traavik, OP Rekvig. Scand J Immunol 1993 Oct;38(4):401-406. 8 of 59 children experienced primary BK virus infection; anti-BK dsDNA antibodies appeared in all 8.

Autoimmunity to DNA and nucleosomes in binary tetracycline-regulated polyomavirus T-Ag transgenic mice. S Bendiksen, M Van Ghelue, T Winkler, U Moens, OP Rekvig. J Immunol 2004 Dec 15;173(12):7630-40.

Acyclic nucleoside phosphonates (acyclovir)

Acyclic nucleoside phosphonates in the chemotherapy of DNA virus and retrovirus infections. E De Clercq. Intervirology 1997;40(5-6):295-303.

Intracellular metabolism of the N7-substituted acyclic nucleoside analog 2-amino-7-(1,3-dihydroxy-2-propoxymethyl) purine, a potent inhibitor of herpesvirus replication. J Neyts, J Balzarini, G Andrei, Z Chaoyong, R Snoeck, A Zimmermann, T Mertens, A Karlsson, E De Clercq. Mol Pharmacol 1998 Jan;53(1):157-165.

Antitumor potential of acyclic nucleoside phosphonates. F De Clercq, G Andrei, J Balzarini, S Hatse, S Liekens, L Naesens, J Neyts, R Snoeck. Nucleosides Nucleotides 1999 Apr-May;18(4-5):759-771.

See Also: Evidence implicating polyomaviruses in birth defects and SIDS as well:

cast 10-28-06