Human parvovirus B19 in patients with aplastic anemia

Mishra, Baijayantimala; Malhotra, Pankaj; Ratho, Radha Kanta; Singh, Mini P.; Varma, Subhash; Varma, Neelam

doi:10.1002/ajh.20347

Cited by 42 publications

(23 citation statements)

References 9 publications

(8 reference statements)

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“…HIV more commonly causes isolated cytopenias but is a very rare cause of AA (Wolf et al, 2007;Hapgood et al, 2013). Likewise, parvovirus B19 is more usually associated with pure red aplasia but has been reported with AA (Mishra et al, 2005) 11. Anti-nuclear antibody and antidouble stranded DNA Pancytopenia in systemic lupus erythematosus may (i) be autoimmune with a cellular bone marrow (ii) associated with myelofibrosis or rarely (iii) with a hypocellular marrow 12.…”

Section: Inherited Aamentioning

confidence: 99%

Guidelines for the diagnosis and management of adult aplastic anaemia

Bown²,

et al. 2015

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Section: Inherited Aamentioning

confidence: 99%

Guidelines for the diagnosis and management of adult aplastic anaemia

Bown²,

et al. 2015

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“…Rare cases of severe aplastic anaemia due to acute Parvovirus B19 infection in individuals without underlying disease have been reported [6][7][8][9][10][11]. An Indian study has documented the presence of Parvovirus B19 IgM and viral DNA in 40.7 and 37% of aplastic anaemia patients, respectively, thereby showing an association of parvovirus infection with aplastic anaemia [12]. Here we have described a previously healthy adult female who presented with vaginal candidiasis, febrile neutropenia and bleeding tendency.…”

Section: Discussionmentioning

confidence: 80%

Acute Parvovirus B19 Infection Leading to Severe Aplastic Anemia in a Previously Healthy Adult Female

Rajput¹,

Sehgal²,

Jain³

et al. 2011

Indian J Hematol Blood Transfus

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Human Parvovirus B19 has been linked to a variety of diseases. One of the most common complications is transient aplastic crisis in patients with chronic hemolytic anemia. Very few case reports have implicated this virus as a putative etiology behind hepatitis and severe aplastic anemia in immuno competent individuals. We report a case of severe aplastic anemia in a previously healthy adult female due to acute parvovirus B19 infection. Laboratory examination showed pancytopenia in peripheral blood and severe hypoplastic bone marrow on biopsy. Serological analysis (ELISA) revealed acute Parvovirus B19 infection. In the face of unavailable HLA matched bone marrow donor, immuno-supressive therapy was contemplated, but could not be given because of financial constraints. Pancytopenia persists till date, 4 months after the diagnosis, with the patient requiring repeated packed red cell and irradiated platelet transfusions. Thus, acute infection with this virus must be considered a cause of acquired aplastic anemia even in individuals without underlying disease.

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“…Bone marrow suppression has been observed subsequent to a number of viral infections, including parvovirus (32, 33), human immunodeficiency virus [HIV; Ref. (34)], viral hepatitis (35), Epstein–Barr virus (36), and influenza (37), among others.…”

Section: Introductionmentioning

confidence: 99%

Hematopoietic Stem Cell Regulation by Type I and II Interferons in the Pathogenesis of Acquired Aplastic Anemia

2016

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Aplastic anemia (AA) occurs when the bone marrow fails to support production of all three lineages of blood cells, which are necessary for tissue oxygenation, infection control, and hemostasis. The etiology of acquired AA is elusive in the vast majority of cases but involves exhaustion of hematopoietic stem cells (HSC), which are usually present in the bone marrow in a dormant state, and are responsible for lifelong production of all cells within the hematopoietic system. This destruction is immune mediated and the role of interferons remains incompletely characterized. Interferon gamma (IFNγ) has been associated with AA and type I IFNs (alpha and beta) are well documented to cause bone marrow aplasia during viral infection. In models of infection and inflammation, IFNγ activates HSCs to differentiate and impairs their ability to self-renew, ultimately leading to HSC exhaustion. Recent evidence demonstrating that IFNγ also impacts the HSC microenvironment or niche, raises new questions regarding how IFNγ impairs HSC function in AA. Immune activation can also elicit type I interferons, which may exert effects both distinct from and overlapping with IFNγ on HSCs. IFNα/β increase HSC proliferation in models of sterile inflammation induced by polyinosinic:polycytidylic acid and lead to BM aplasia during viral infection. Moreover, patients being treated with IFNα exhibit cytopenias, in part due to BM suppression. Herein, we review the current understanding of how interferons contribute to the pathogenesis of acquired AA, and we explore additional potential mechanisms by which interferons directly and indirectly impair HSCs. A comprehensive understanding of how interferons impact hematopoiesis is necessary in order to identify novel therapeutic approaches for treating AA patients.

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Human parvovirus B19 in patients with aplastic anemia

Cited by 42 publications

References 9 publications

Guidelines for the diagnosis and management of adult aplastic anaemia

Guidelines for the diagnosis and management of adult aplastic anaemia

Acute Parvovirus B19 Infection Leading to Severe Aplastic Anemia in a Previously Healthy Adult Female

Hematopoietic Stem Cell Regulation by Type I and II Interferons in the Pathogenesis of Acquired Aplastic Anemia

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