Preliminary CommunicationsPARVOVIRUS-LIKE PARTICLES IN HUMAN SERA
Abstract
A parvovirus-like antigen has been found in sera of nine healthy blood-donors and two patients. Its pathogenicity is unknown, but 30% of adults possess specific antibody. The new agent can be confused with hepatitis-B antigen both morphologically and serologically.
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Cited by (799)
Parvovirus B19 infection after kidney transplantation: A single centre experience
2023, Medical Journal Armed Forces IndiaParvovirus B19 is an uncommon cause of anaemia in kidney transplant recipients (KTRs). The study aims to determine the incidence, clinical presentation, laboratory findings and outcome of parvovirus B19-related anaemia in KTR.
We conducted a 12-year retrospective, single-centre study describing the clinical profile of KTRs with parvovirus B19-related anaemia.
Amongst the 714 patients who underwent kidney transplantation between January 2011 and January 2023, (cumulative follow-up: 1287 patient-years), six females and one male, developed parvovirus B19-related anaemia. The incidence proportion (risk) is 0.98% with an incidence rate of 5.43 cases per 1000 patient-year. The median duration from transplant to development of anaemia was 6 weeks (range: 4–40 weeks). The mean fall in haemoglobin was 2.88 ± 1.55 gm/dl; concomitant leukopenia and thrombocytopenia were observed in 57.1 and 28.6% of patients. Three patients responded to a reduction in immunosuppression, the four non-responders required the administration of low-dose intravenous immunoglobulin. The mean duration from initiation of therapy to a sustained rise in haemoglobin was 7.71 ± 2.62 weeks. None of the patients had a relapse of the infection.
Parvovirus B19 infection is an uncommon cause of post-transplant refractory anaemia. The key to successfully managing such patients includes a high index of suspicion, early diagnosis and reduction of immunosuppression with or without administration of intravenous immunoglobulin.
Parvovirus B19 infections in adults
2022, Revue de Medecine InterneL’infection aiguë à Parvovirus B19 (PVB19), responsable du mégalérythème épidémique de l’enfant, entraîne chez l’adulte immunocompétent des polyarthralgies aspécifiques associées à des lésions cutanées et des manifestations plus rares (hépatiques, neurologiques, cardiaques ou néphrologiques). Chez l’immunodéprimé, les cytopénies sont plus fréquentes et dans certains cas la virémie persiste et est responsable d’une infection chronique à PVB19. Le PVB19 est également à l’origine de crises érythroblastopéniques au cours de maladies hémolytiques chroniques. L’infection aiguë à PVB19 est un diagnostic différentiel de certaines maladies auto-immunes et a été suspecté comme agent déclenchant de certaines pathologies auto-immunes du fait de sa capacité à favoriser l’émergence de marqueurs d’auto-immunité. Des mécanismes de mimétisme moléculaire, d’induction d’apoptose et d’activation de certaines enzymes ont été démontrés, expliquant en partie la production d’auto-anticorps au cours de l’infection. La démonstration d’une relation causale dans le déclenchement de maladie auto-immune reste cependant à réaliser. Cette mise au point propose une synthèse des données cliniques de l’infection à PVB19 chez l’adulte avec un focus particulier sur ces liens avec l’auto-immunité.
Acute Parvovirus B19 (PVB19) infection is responsible for erythema infectiosum in children and non-specific polyarthralgias in immunocompetent adults associated with skin lesions and rarer manifestations (hepatic, neurological, cardiac or nephrological). In immunocompromised patients, cytopenias are more frequent and in some cases, viremia persists and is responsible for PVB19 chronic infection. PVB19 is responsible for pure red cell aplasia during chronic hemolytic diseases. Acute PVB19 infection is a differential diagnosis of some autoimmune diseases and has been suspected to be a trigger for some autoimmune diseases because of its ability to promote the emergence of autoimmune markers. Mechanisms of molecular mimicry, induction of apoptosis and activation of enzymes have been demonstrated, explaining in part the production of autoantibodies during infection. However, the demonstration of a causal relationship in the triggering of autoimmune disease remains to be done. This review provides a synthesis of the PVB19 infection clinical data in adults with a particular focus on these links with autoimmunity.
Parvovirus B19 infection in kidney transplant recipients: A prospective study in a teaching hospital in Shanghai, China
2022, Transplant ImmunologyThere is a lack of epidemiological studies on the course and clinical characteristics of Parvovirus B19 (B19V) infections in kidney transplant (KT) recipients. This study was undertaken to provide recommendations for clinical B19V infection diagnosis and treatment.
Serum samples of KT recipients were regularly collected and tested for B19V-DNA copies, B19V-IgG/IgM levels, as well as hematological parameters and functions of kidney and liver. The course of B19V infection was described according to the results of serology and DNA testing, and the clinical and epidemiological data were combined for analysis.
75% B19V infections occurred within 2 weeks after KT(n = 9). The infection rate of B19V in KT recipients was high, namely 10.17% (n = 12). The number of 10 patients IgM antibodies against B19V (IgM+) and the DNA B19V (DNA+), whereas 2 patients were IgM negative (IgM-) but DNA+. The B19V infected KT patients showed several symptoms, including anemia (100%), reduction of platelets (8.33%), and damage to liver (75%) and kidney function (16.67%) Patients with progressive anemia in the first two weeks after KT, which combined with the decrease of reticulocytes, are more likely to have B19V infection. Associations of four main therapeutic risk factors for B19V infections in KT patients have been analyzed. B19V infection was associated with use of basiliximab (OR = 1.19; 95%- CI: 1.08–1.32; P = 0.003) and use of thymoglobulins (OR = 0.84; 95%-CI: 0.76–0.93; P = 0.003).
Doctors should be alert to B19V infection, especially in the immunodeficient patients within the first two weeks after transplantation.
Aplastic anemia induced by human parvovirus B19 infection in an immunocompetent adult male without prior hematological disorders: A case report
2022, Annals of Medicine and SurgeryParvovirus B19 (B19V) is a human pathogenic virus of clinical relevance. Human parvovirus B19 infection can be asymptomatic or frequently associated with erythema infectiosum, or joint symptoms in healthy adults. Aplastic anemia as a complication of human parvovirus infection is rare in healthy adults without prior hematological disorders.
We report a case of severe aplastic anemia in a 22-years-old immunocompetent adult male without any hematological dysfunction who presented with periumbilical pain, loose watery stools, and fever with chills and rigor. General examination, laboratory investigation, and peripheral blood smear revealed anemia with leucopenia and relative lymphocytosis, thrombocytopenia, and severe neutropenia. Bone marrow biopsy revealed hypocellular bone marrow with maturation arrest at the proerythroblast stage with intranuclear inclusions and no blast and hematopoietic cells replaced by mature adipocytes in marrow spaces. Parvovirus B19 infection was confirmed by viral serology and polymerase chain reaction.
Asymptomatic or mild infection occurs most often when B19 affects immunocompetent adults. However, this is the fourth case reporting severe aplastic anemia in immunocompetent adults and the first case reported in immunocompetent adult males. The patient was admitted for close monitoring and supportive management, which effectively improved the patient's clinical condition, and discharged with a strict follow-up schedule in an outpatient setting.
Thus, acute infection with this virus must be considered a cause of acquired aplastic anemia even in individuals without underlying disease.
Parvovirus B19: a Clinical and Diagnostic Review
2022, Clinical Microbiology NewsletterCitation Excerpt :The name parvovirus B19 was used because the virus was found by electron microscopy in serum number 19 of panel B. This serum yielded a positive counter-immunoelectrophoresis result but a negative radioimmunoassay result for HBV surface antigen, leading to the conclusion that the immunoelectrophoresis result was falsely reactive [2]. Five years later, the virus was independently described in Japan as the Nakatani virus [3].
Parvovirus B19 is a small, non-enveloped, single-stranded DNA virus with global distribution. It is primarily known for being the causative agent of fifth disease, also known as erythema infectiosum, a common self-limiting childhood disease characterized by the development of a rash. During infection, it targets erythroid progenitor cells in bone marrow, where it replicates and ultimately induces cellular apoptosis. In the correct patient population, it may be responsible for the development of arthropathy, aplastic crisis, nonimmune hydrops fetalis, viral-associated hepatitis, and myocarditis. However, most infections are asymptomatic and remain undetected. Here, we review the nature of this virus to provide information about its biology; interactions with the human host; how those interactions shape the clinical presentation; and, finally, the available diagnostic approaches.
The detection, treatment of parvovirus B19 infection induced anemia in solid organ transplants: A case series and literature review of 194 patients
2022, Transfusion Clinique et BiologiqueThere are no optimal diagnostic, treatment and post-infection surveillance strategies for parvovirus B19 infection in solid organ transplantation (SOT) recipients.
We conducted a retrospective review of all PVB19 infected cases confirmed by qPCR among SOT recipients at our institution over a 3-year period and reviewed the literature from 1990 to 2021.
Eight kidney and two heart transplant patients with refractory anemia had PVB19 infection. The viral DNA load in peripheral blood ranged from 2.62 × 102 to 8.31 × 106 copies/mL. Two patients with the lowest PVB19 DNA load only reduced the use of immunosuppressants and anemia was relieved. Eight received intravenous immunoglobulin (IVIG) (ranging from 0.25 to 0.5 g/kg/day). The median time to anemia improvement (hemoglobulin > 100 g/L) was 16 days (8–70 days) after treatment. One patient had a PVB19 relapse and viral DNA load > 1.00 × 108 copies/mL at diagnosis. A total of 86 studies involving 194 SOTs were screened from the literature, and the most common symptom was anemia and low reticulocyte count. PVB19 DNA was detected in all cases. Of that, 91.4% of cases received IVIG, 53.8% received IVIG and immunosuppression reduction, 6.5% of cases showed reduced immunosuppression without IVIG, and 2.1% did not receive any special treatment. The recurrence rate was 17.5%.
PVB19 infection is a cause of anemia after SOT, and treatment mainly relies on IVIG and/or immunosuppression reduction.