Multiple sclerosis-associated virus-related pol sequences found both in multiple sclerosis and healthy donors are more frequently expressed in multiple sclerosis patients.

In the etiopathogenesis of multiple sclerosis (MS), both genetic and environmental factors play an important role. Among environmental factors, viral infections are most likely connected with the etiology of MS. There are many evidence suggesting possible involvement of retroviruses in the development of autoimmune diseases including MS. Multiple sclerosis-associated retrovirus (MSRV) seems to be the important candidate for viral etiology of MS. The aim of the study was to analyze MSRV pol sequences in patients with MS. As control, groups of myasthenia gravis, Parkinson's disease, and migraine patients, and healthy individuals have been studied. The MSRV pol sequences have been analyzed in RNA isolated from the serum and in DNA and RNA of peripheral blood lymphocytes from untreated MS patients and control groups. The MSRV pol sequences have been detected by reverse transcriptase-polymerase chain reaction (RT-PCR) and PCR technique, using specific oligonucleotide primers. In the serum RNA (cDNA), MSRV pol sequences have been identified in 31/32 MS patients. MSRV pol sequences were detected in serum cDNA of 9/17 myasthenia gravis patients, 7/16 Parkinson's disease patients, 10/21 migraine patients, and 13/27 healthy individuals. MSRV pol sequences were observed also in RNA from lymphocytes of all MS patients, 12/17 myasthenia gravis patients, 9/16 Parkinson's disease patients, 14/21 migraine patients, and 18/27 healthy donors. In the DNA from peripheral blood lymphocytes of all studied patients and healthy individuals, MSRV pol sequences have been found. The observed pattern of fiber-fluorescence in situ hybridization (FISH) signals suggests the presence of multiple copies of MSRV pol sequences, most likely tandemly dispersed in the genome. It can be concluded that MSRV pol sequences are endogenous, widespread in lymphocytes DNA, and transcribed into RNA of MS patients as well as of other studied patients and healthy individuals. However, more frequent expression of MSRV sequences detected in lymphocytes RNA (cDNA), as well as their presence in higher frequency in the serum of MS patients, may suggest the involvement of MSRV in the etiopathogenesis on MS.

[Role of TT virus in pathogenesis of liver diseases--the prevalence of TTV in patients and healthy individuals]. / Rola wirusa TT w patogenezie chorób watroby--analiza wystepowania TTV u osób chorych i zdrowych.

Primarily TTV has been thought as an etiologic agent of post transfusion non-A to -G hepatitis. TTV can replicate in liver and bone marrow cells. The presence of TTV has been found in the serum of patients with acute as well as chronic hepatitis of known etiology. Patients with acute hepatitis A, B, C and hepatitis caused by EBV or CMV all have TTV viremia in a frequency up to 60%. In chronic viral hepatitis TTV was present in a wide range of 7-94.4%. Treatment of viral hepatitis patients with interferon alfa and rybawiryn leads to eradication of TTV viremia in 50% cases. TTV infection in hepatocellular carcinoma ranged from 8.1% up to 100% patients. In hepatitis of unknown etiology TTV infection was observed in 26% to 71% cases. In liver cirrhosis TTV infection has been evidenced in 10% to 66% patients. Some authors postulated that the frequency of TTV increased with the number of blood or blood products transfusions. Coinfection of TTV has been found in 34.9%-76% of HIV positive persons. The study of medical staff revealed no difference in TTV viremia with healthy individual control. TTV is widespread in healthy general population. Therefore based on so far published results the association between TTV infection and hepatitis is questionable.

[TT virus--characteristics, occurrence and routes of transmission]. / Wlasciwosci, wystepowanie i drogi przenoszenia wirusa TT.

Recent discovery of a novel DNA virus from the serum of a Japanese patient (T.T.) has prompted further studies directed on possible role of TT virus in the development of cryptogenic hepatitis. The TT is an unenveloped and circular DNA virus. TTV possesses single stranded DNA genome and comprises 3537 to 3853 nucleotides. TTV is similar to the Circoviridae and possesses three open reading frames. Phylogenetic analysis revealed up to 30% nucleotide sequence divergence in the 16 virus genotypes. TTV infection can be detected by polymerase chain reactions, in situ hybridization and by specific antibodies to TTV. TTV DNA has been identified in the serum of patients with cryptogenic hepatitis, hepatitis B and C, hepatocellular carcinoma as well as in healthy individuals. TTV has been found also in the peripheral blood leukocytes, bone marrow cells, liver biopsies as well as in feces and breast milk. Some animals including cattle, sheep, pigs and chicken appeared to have TTV viremia. Recent detection of TTV in nonblood products, such as saliva and feces suggest in addition to parenteral also nonparenteral routes of TTV transmissions including sexual and fecal-oral.

[Prevalence of TT virus in patients with hepatitis B,C and hepatitis of unknown etiology]. / Wystepowanie wirusa TT u chorych z zapaleniem watroby typu B, C i o nieustalonej etiologii.

Discovery of TT virus in 1997 gave raise to intensive subsequent studies to learn about its structure, features and, what is the most important, about its role in pathogenesis of liver disease. The aim of the work was to analyze prevalence of TTV DNA in patients with diagnosed hepatitis B, C, that of unknown etiology and in healthy blood donors as well. Additionally the divergence of TTV sequence was estimated in selected cases. TTV DNA was detected by PCR technique using specific oligonucleotide primers for coding regions. TT virus has been detected in 25.6% (32/125) HBsAg positive patients and in 23.9% (51/213) HCV infected patients. In healthy blood donors the frequency of TTV was 24.3% (34/140) similarly to that found in HCV and HBV infected patients. The frequency of TTV DNA among patients with hepatitis of unknown etiology was 9.1%. This result was statistically significant lower than in the other groups. When detected sequences have been compared to these from NCBI base the homology result was 71% to 95%, and among different patients and groups of patients identity was 46% to 73%. On the basis of the obtained results it can be concluded that it is very unlikely that TTV coinfection plays any significant role in HCV or HBV infection. The hypothetical role of TTV infection in the etiopathogenesis of cryptogenic chronic hepatitis has not been confirmed. The results obtained in the small group of patients with hepatitis of unknown etiology are not conclusive and should be taken with some precaution. The final conclusion is the TTV coinfection does not contribute to the liver pathology. The divergence of TTV sequences may explain the various frequency of TTV viremia reported by other authors.