The association of myelodysplasia with autoimmunity is well established for almost 20 years and has been confirmed by clinical and laboratory data [5, 6].
There are several reports in the literature correlating various autoimmune manifestations such as leukocytoclastic vasculitis , relapsing polychondritis , polyarteritis nodosa, Grave's disease, Sjögren's syndrome , Wegener's granulomatosis , bronchiolitis obliterans , autoimmune hemolytic anemia , and thrombocytopenia [13, 14], red cell aplasia , dermatomyositis , peripheral polyneuropathy and inflammatory bowel disease , giant cell arteritis/polymyalgia rheumatica [18, 19], and Addison's disease .
MDSs have been linked to several types of glomerular diseases, such as glomerulosclerosis, membranous nephropathy, IgA nephropathy, and ANCA associated nephropathy [21–25]. Unfortunately, in our case, due to lack of histopathologic examination, only speculations can be made about the type of the patient's renal disease.
Both the innate and adoptive immune system have been implicated in the autoimmune manifestations of patients with MDS in several studies evaluating T cell activation, function, and kinetics, as well as associations with the HLA system [26, 27].
A large number of reports favor the use of immunoregulatory treatments  such as antithymocyte globuline, cyclosporine, thalidomide, steroids, mycophenolate mofetil, anti-TNF, and methotrexate in patients with MDS and autoimmune manifestations. More recently, guidelines for the use of immunomodulatory treatment for MDS have been proposed .
In our case, myelodysplastic syndrome and autoimmune phenomena were also accompanied by a positive PCR for HTLV-1. HTLV-1 has been implicated in the pathogenesis of ATLL and tropical spastic paraparesis. Although the virus is oncogenic, it neither induces oncogenesis by encoding oncogenes, nor does it integrate into the host genome to disrupt host gene expression. Rather, viral gene products interact with host proteins (mainly transcription factors) altering their function.
It is estimated that 10-20 million people are infected by the virus worldwide. In endemic areas (southern Japan, the Caribbean, South America, the Melanesian islands, Papua New Guinea, the Middle East and central and southern Africa) seroprevalence ranges from 3% to 30%. In non-endemic areas, such as Greece, seroprevalence is less than 1%. Seropositivity among blood donors in Greece was reported to be 0.009% in a large multicenter study .
Transmission of the virus is mainly achieved through breast feeding, sexual intercourse, inappropriate sterilization procedures and blood transfusion or injection drug use. Our patient claimed not to be an injection drug user, and had never been transfused in the past. His wife tested negative for HTLV-1.
In the literature serologic positivity for the virus has been detected in patients with myelodysplastic syndromes in both endemic  and non endemic regions for the virus .
Most studies about the prevalence of HTLV-1 in hematologic diseases come from Japan where the infection is endemic. Several case reports suggest the possible association between immune thrombocytopenia (ITP) and HTLV-1 infection . Recently Inoue et al. studied HTLV-1 prevalence in patients with RAEB/RAEBt and AML . The high prevalence (28.3%) of HTLV-1 infection in the studied group of patients with RAEB/RAEBt is very interesting but cannot be extrapolated to patients of non-endemic regions. There is only one study in the literature coming from a non endemic region that suggests a possible role of HTLV-1 infection in the pathogenesis of hematologic diseases other than ATLL, especially MDS .
Association of the virus with rheumatologic manifestations is not rare and includes uveitis, chronic inflammatory arthropathy, Sjögren's syndrome, lymphocytic alveolitis, polymyositis, and fibromyalgia, but all these reports come from regions endemic for the HTLV-1 infection [33–40]. Moreover, there are 3 reports, coming from endemic regions, associating HTLV-1 with glomerulonephritis and interstitial nephritis [35, 41, 42].
Treatment of the diseases caused by HTLV-1 is problematic. There have been only limited studies of specific antiretroviral therapy using nucleoside analogue reverse transcriptase inhibitors for HTLV-1 infection [43–45].
Azacytidine and its deoxy derivative, decitabine (5-aza-2'deoxycytidine), are FDA-approved agents for the treatment of low and high risk patients with MDS. Azacytidine is incorporated into DNA and RNA by methyltransferases and acts as a false substrate and a potent inhibitor of methyltransferases. This results in reduction of DNA methylation (hypomethylating or demethylating agent) affecting the binding of cell regulation proteins to the DNA/RNA substrate [46, 47]. DNA hypermethylation at the CpG islands has been described in MDS. These CpG islands are targets for transformation-associated aberrant hypermethylation activity during leukemogenesis. Moreover, aberrant CpG island hypermethylation seems to be an important multistep process in the development of ATLL .
It has been shown that 5-azacytidine inhibits human immunodeficiency virus type 1 (HIV-1) replication . This antiviral activity can be attributed to an increase in the frequency of viral mutants, achieved by incorporation of its derivative 5-aza-2'-deoxycytidine into the viral DNA. The same may apply to other retroviruses such as HTLV-1, for which it has been shown that its transcriptional activity is regulated by methylation . Recently, a closely related molecule, decitabine, has been successfully used in a trial to reduce HIV infectivity . The antiviral activity of the drug has been attributed to an increase in the mutational load that inhibits the generation of infectious progeny virus from provirus.
The antiretroviral activities of hypomethylating factors, such as decitabine and 5-azacytidin are the subject of several current studies. One of them suggests a more specific role of 5-azacytidine in the treatment of ATLL, as it shows a growth inhibition of leukemic cells, offering a potential new therapeutic approach to improve the poor outcomes associated with ATLL .
Although in our case, HTLV-1 negativity may have resulted from other unidentified factors, such as immune restoration following treatment, our case may be another example of drug repositioning, were azacitidine administered to treat MDS, had also an effect on HTLV-1 replication, resulting into a negative PCR for the virus several months following treatment.