6
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      HERV-K and HERV-W transcriptional activity in myalgic encephalomyelitis/chronic fatigue syndrome

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/MS) is an incapacitating chronic disease that dramatically compromise the life quality. The CFS/ME pathogenesis is multifactorial, and it is believed that immunological, metabolic and environmental factors play a role. It is well documented an increased activity of Human endogenous retroviruses (HERVs) from different families in autoimmune and neurological diseases, making these elements good candidates for biomarkers or even triggers for such diseases.

          Methods

          Here the expression of Endogenous retroviruses K and W (HERV-K and HERV-W) was determined in blood from moderately and severely affected ME/CFS patients through real time PCR.

          Results

          HERV-K was overexpressed only in moderately affected individuals but HERV-W showed no difference.

          Conclusions

          This is the first report about HERV-K differential expression in moderate ME/CFS. Although the relationship between HERVs and ME/CFS has yet to be proven, the observation of this phenomenon deserves further attention.

          Related collections

          Most cited references14

          • Record: found
          • Abstract: found
          • Article: found
          Is Open Access

          Chronic viral infections in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)

          Background and main text Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex and controversial clinical condition without having established causative factors. Increasing numbers of cases during past decade have created awareness among patients as well as healthcare professionals. Chronic viral infection as a cause of ME/CFS has long been debated. However, lack of large studies involving well-designed patient groups and validated experimental set ups have hindered our knowledge about this disease. Moreover, recent developments regarding molecular mechanism of pathogenesis of various infectious agents cast doubts over validity of several of the past studies. Conclusions This review aims to compile all the studies done so far to investigate various viral agents that could be associated with ME/CFS. Furthermore, we suggest strategies to better design future studies on the role of viral infections in ME/CFS.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: found
            Is Open Access

            The discovery of endogenous retroviruses

            When endogenous retroviruses (ERV) were discovered in the late 1960s, the Mendelian inheritance of retroviral genomes by their hosts was an entirely new concept. Indeed Howard M Temin's DNA provirus hypothesis enunciated in 1964 was not generally accepted, and reverse transcriptase was yet to be discovered. Nonetheless, the evidence that we accrued in the pre-molecular era has stood the test of time, and our hypothesis on ERV, which one reviewer described as 'impossible', proved to be correct. Here I recount some of the key observations in birds and mammals that led to the discovery of ERV, and comment on their evolution, cross-species dispersion, and what remains to be elucidated.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Placental syncytins: Genetic disjunction between the fusogenic and immunosuppressive activity of retroviral envelope proteins.

              We have previously demonstrated that the envelope proteins of a murine and primate retrovirus are immunosuppressive in vivo. This property was manifested by the ability of the proteins, when expressed by allogeneic tumor cells normally rejected by engrafted mice, to have the env-expressing cells escape (at least transiently) immune rejection. Here, we analyzed the immunosuppressive activity of the human and murine syncytins. These are envelope genes from endogenous retroviruses independently coopted by ancestral hosts, conserved in evolution, specifically expressed in the placenta, and with a cell-cell fusogenic activity likely contributing to placenta morphogenesis. We show that in both humans and mice, one of the two syncytins (human syncytin-2 and mouse syncytin-B) is immunosuppressive and, rather unexpectedly, the other (human syncytin-1 and mouse syncytin-A) is not (albeit able to induce cell-cell fusion). Delineation of the immunosuppressive domain by deletion analysis, combined with a comparison between immunosuppressive and nonimmunosuppressive sequences, allowed us to derive a mutation rule targeted to specific amino acids, resulting in selective switch from immunosuppressive to nonimmunosuppressive envelope proteins and vice versa. These results unravel a critical function of retroviral envelopes, not necessarily "individually" selected for in the retrovirus endogenization process, albeit "tandemly" conserved in evolution for the syncytin pairs in primates and Muridae. Selective inactivation of immunosuppression, under conditions not affecting fusogenicity, should be important for understanding the role of this function in placental physiology and maternofetal tolerance.
                Bookmark

                Author and article information

                Contributors
                +55 11 3061-8668 , cmromano@usp.br
                Journal
                Auto Immun Highlights
                Auto Immun Highlights
                Autoimmunity Highlights
                BioMed Central (London )
                2038-0305
                2038-3274
                15 November 2019
                15 November 2019
                December 2019
                : 10
                : 1
                : 12
                Affiliations
                [1 ]ISNI 0000 0004 1937 0722, GRID grid.11899.38, Laboratório de Virologia, Instituto de Medicina Tropical de São Paulo, , Universidade de São Paulo, ; Rua Dr. Enéas de Carvalho Aguiar, 470, São Paulo, SP 05403-000 Brazil
                [2 ]ISNI 0000 0001 0106 6835, GRID grid.412283.e, Pós-Graduação em Ciências da Saúde, , Universidade Santo Amaro, ; São Paulo, Brazil
                [3 ]ISNI 0000 0004 1937 0722, GRID grid.11899.38, Departamento de Moléstias Infecciosas e Parasitárias, , Faculdade de Medicina da Universidade de São Paulo, ; São Paulo, Brazil
                [4 ]ISNI 0000 0004 0425 469X, GRID grid.8991.9, Department of Clinical Research, Faculty of Infectious and Tropical Diseases, , London School of Hygiene and Tropical Medicine, ; London, UK
                [5 ]ISNI 0000 0004 1937 0722, GRID grid.11899.38, Hospital das Clinicas HCFMUSP (LIM52), Faculdade de Medicina, , Universidade de São Paulo, ; São Paulo, Brazil
                Author information
                http://orcid.org/0000-0003-4550-1987
                Article
                122
                10.1186/s13317-019-0122-8
                7065355
                1f95af58-3b73-43c4-a761-d836ca3c8cbe
                © The Author(s) 2019

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                : 3 September 2019
                : 9 October 2019
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100001807, Fundação de Amparo à Pesquisa do Estado de São Paulo;
                Award ID: 2015/05958-3
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/100000002, National Institutes of Health;
                Award ID: 2R01AI103629
                Award Recipient :
                Funded by: Programa de fomento às atividades de lideranças científicas dos LIMs do Hospital das Clínicas da FMUSP (PROFAP-LIM/HCFMUSP)
                Award ID: 26/2019
                Award Recipient :
                Categories
                Original Research
                Custom metadata
                © The Author(s) 2019

                endogenous retroviruses,herv-w,herv-k,myalgic encephalomyelitis,chronic fatigue

                Comments

                Comment on this article