Was. Up until about the early 90s yes there could be legit debate. Now the case for the link between HIV and AIDs is far far to solid:
niaid.nih.gov/factsheets/howhiv.htm
Well, whether they are wrong or right - as my own analysis of the data isnt finished yet, i just cant say - in any case, duesberg et al wont agree:
The chemical bases of the various AIDS epidemics: recreational
drugs, anti-viral chemotherapy and malnutrition
PETER DUESBERG†, CLAUS KOEHNLEIN* and DAVID RASNICK
J. Biosci. | Vol. 28 | No. 4 | June 2003 | 383–412 |
h**p://*ww.virusmyth.net/aids/data/pddrchemical.pdf
But here is something else i want to present, its related to above study on SLE, who found that both patients and mice with induced SLE very often test positive for HIV:
Rheumatology 2000; 39: 1047-1048
© 2000 British Society for Rheumatology
Letters to the Editor
Presence of HIV infection in patients diagnosed with systemic lupus erythematosus
D. J. Clutterbuck, J. Watson1, A. De Ruiter1, T. Godfrey2 and C. Bradbeer1
Department of GU Medicine, Level 1, Lauriston Building, Lauriston Place, Edinburgh EH3 9YW and
1 Department of GU Medicine and
2 Louise Coote Lupus Unit St. Thomas' Hospital, London, SE1 7EH, UK
SIR, Young females, the population in whom systemic lupus erythematosus (SLE) is most commonly diagnosed, are not regarded as being at high risk of HIV infection in the UK. We describe two cases in which a diagnosis of seronegative SLE was made on clinical grounds some time before the detection of HIV infection.
Case 1 was a 35-yr-old white Colombian-born woman who presented in November 1996 with knee and elbow pain, dry eyes and mouth and symptoms suggestive of Raynaud's phenomenon. She had been diagnosed with SLE elsewhere in 1995, when she had been found to have a florid butterfly rash and hair loss. Investigations revealed an erythrocyte sedimentation rate (ESR) of 88 mm/h, a low C4 level and lymphopenia of 0.8 x 109/l (normal value >1.5 x 109/l). Antinuclear antibodies (ANA), anti-double-stranded DNA (anti-dsDNA), antiphospholipid antibody and lupus anticoagulant were negative. The diagnosis of active seronegative SLE was agreed and prednisolone was added to her hydroxychloroquine therapy. She developed difficulty in walking. MRI appearances were felt to be suggestive of transverse myelitis. She was treated with pulse cyclophosphamide and prednisolone and later azathioprine. She developed dysarthria, dysphagia and urinary retention, and at this stage had finger–nose ataxia and horizontal nystagmus in addition to spastic paraparesis, with no evidence of a sensory level. Cerebrospinal fluid (CSF) findings were consistent with inflammatory myelopathy. At this time she had oesophageal candidiasis, chronic, pathogen-negative diarrhoea and orolabial herpes. She had lost 7 kg in weight.
Pancytopenia persisted despite discontinuation of azathioprine. When bone marrow trephine revealed mycobacteria she underwent an HIV test, which was HIV-1 antibody-positive. The CD4 count was 1/mm3. CSF contained cytomegalovirus, herpes simplex virus, varicella zoster virus and Mycobacterium avium intracellulare (MAI). With antiviral, antimycobacterial and antiretroviral therapy, there was limited improvement in her confusion but no improvement in spastic paraparesis. She had had no malar rash or arthralgia for over 1 yr after starting HIV/AIDS antiretroviral therapy (HAART). She died in July 1999.
Case 2 was a 44-yr-old, single, white, UK-born woman who was seen by an oral surgeon with a history of oral ulceration, loss of taste, a tender tongue, fatigue, patchy alopecia and amenorrhoea. Her only significant medical history was of a single epileptic seizure, after which she had been commenced on sodium valproate 600 mg daily. At that time she had developed some dysphagia and vaginal soreness and had lost 13 kg in weight. She was noted to have generalized erythema of the palate and buccal gingivae, cervical lymphadenopathy and ulcers at the vaginal introitus. Investigations revealed a normal haemoglobin concentration, platelet count and total white blood count, with mild lymphopenia (1.4 x 109/l) and a raised ESR of 56 mm/h. Renal and liver function tests were normal. ANA were negative and C3 was normal but C4 was low. IgG, IgA and IgM were raised. Biopsy of oral mucosa showed microulceration with a dense lymphocytic infiltrate and a single fungal hypha. The appearances were consistent with the clinical diagnosis of seronegative SLE. The patient was referred to a rheumatologist, but before being seen she attended the emergency department with right lobar pneumonia. Bronchoscopy revealed the presence of multidrug-resistant Mycobacterium tuberculosis and Pneumocystis carinii in bronchial washings. She tested positive for HIV antibody. Her CD4 count was 20/mm3. Six-drug anti-tuberculous therapy and HAART was initiated. She has had no oral ulceration or rash for over 1 yr.
There are many similarities between the clinical and laboratory manifestations of systemic lupus erythematosus (SLE) and those of HIV infection. Very few cases have been reported of the coexistence of SLE and HIV in the same individual [1], which appears to occur far less commonly than the relative prevalences of the two diseases would lead us to predict [2].
SLE involves disease of the lymphoid organs, skin, joints, central nervous system, kidneys and lungs, as does HIV. Malar rash, oral ulceration, sicca syndromes, alopecia, arthralgia and arthritis, fever and neuropathies are features of both conditions [3]. A number of laboratory findings may occur in both diseases, including leukopenia, lymphopenia, hypergammaglobulinaemia and the presence of antiphospholipid antibodies. ANA and rheumatoid factor occur, albeit less frequently, in HIV-infected individuals, but the presence of anti-dsDNA has not been described [4].
In both of the above cases, laboratory findings showed raised ESR, low C4 levels and negative ANA. Symptoms and signs at presentation suggested SLE, and in case 1 the patient fulfilled the ARA criteria for SLE. Both individuals were single, white women with a low number of sexual partners and no history of injecting drug use. A retrospective review of risk factors revealed that heterosexual intercourse in the UK was the probable mode of acquisition in both women. As heterosexual transmission of HIV now accounts for the largest proportion of new HIV diagnoses in the UK, it cannot be excluded in young women on the grounds of lack of risk factors alone. The test should be considered particularly in seronegative SLE, which accounts for less than 5% of SLE diagnoses [5], and before the institution of immunosuppressive therapy.
My Comment: Compare that to the first study. These patiernt where put on - very toxic ARV - and where presumed to be HIV - infected , although SLE patients very frequently test positive anyway (according to the first study). Of course the author muses over why this person have contracted hiv anyway with only a low number of lifetime sexual partners... The first person died on HAART, i note he didnt say what caused the death. Number one killer on HAART is liver failure (although its true that people on HAART live longer as they did on AZT back in the '80 - but, sadly, there is, as far as i know no placebo-controlled study, both for HAART and AZT-Monotherapy, so the fact that they now live longer could be just due to less toxicity of HAART)
comments welcome.
still analyzing...
