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Sharma K, Khandia R, Shrivastava R, Nema RK, Mishra S, Kanwar RK, Raut AA, Agrawal A, Gupta V, Pandey MK. Exploring the link between parvovirus B19 and encephalitis: a systematic review and comprehensive meta-analysis of molecular and serological evidence. Virol J 2025; 22:42. [PMID: 39972487 PMCID: PMC11837615 DOI: 10.1186/s12985-025-02630-z] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/05/2024] [Accepted: 01/13/2025] [Indexed: 02/21/2025] Open
Abstract
Encephalitis, a severe brain inflammation, can arise due to various infectious agents, including viruses like Parvovirus B19 (B19V). Previously linked to mild neonatal and young one's illnesses and some haematological diseases, recent evidence associates B19V with encephalitis, with no clear prevalence and mechanisms in place. This systematic review and meta-analysis aim to determine the prevalence of B19V in cases of encephalitis, exploring variations associated with diagnostic approaches, and identifying gaps in existing research to enhance clinical comprehension and diagnostic methods. An extensive search (1994-2024) was performed through PubMed, Scopus, ScienceDirect, and Cochrane databases for research and epidemiological investigations related to B19V in cases of encephalitis. Inclusion criteria focused on studies that verified B19V using molecular (PCR, NGS) or serological (IgM/IgG) techniques in cerebrospinal fluid or serum. Data analysis was done to pool the prevalence data of included studies using a random-effects model. Heterogeneity was evaluated using I2 statistics. Sensitivity and meta-regression analyses were conducted to evaluate variability and the effects of moderators. A total of fourteen studies involving 3,135 encephalitis patients resulted in a combined prevalence of 3% (95% CI: 2-4%). Studies using PCR indicated a greater prevalence (3%) in comparison to ELISA (1%) and NGS (2%). A moderate level of heterogeneity (I2 = 57.4%) was attributed to the variability in diagnostic methods and geographic distribution. Sensitivity analyses validated strong estimates, while meta-regression revealed country as a key moderator accounting for heterogeneity. Publication bias was modest. The research indicates that B19V may be involved in certain encephalitis instances, with an overall prevalence of 3%. The differences observed in the studies emphasize the need for standardized diagnostic procedures and more extensive multicentric epidemiological research.
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Affiliation(s)
- Kashmi Sharma
- Department of Translational Medicine, AIIMS Bhopal, Bhopal, India
| | - Rekha Khandia
- Department of Genetics, Barkatullah University, Bhopal, MP, India
| | | | | | - Somesh Mishra
- Department of Translational Medicine, AIIMS Bhopal, Bhopal, India
| | | | | | - Amit Agrawal
- Department of Neurosurgery, AIIMS Bhopal, Bhopal, India.
| | - Vandana Gupta
- Department of Microbiology, NDVSU, Jabalpur, MP, India
| | - Megha K Pandey
- Department of Translational Medicine, AIIMS Bhopal, Bhopal, India.
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Kn SK, Chellapuram SK, Ganguly S, Pushpam D, Giri RK, Bakhshi S. Early stoppage of empirical antibiotic therapy at clinical improvement in paediatric leukaemia patients with high-risk febrile neutropenia (ESAT-HR-FN study): Study protocol of a single centre investigator initiated randomised open label non-inferiority trial. Heliyon 2024; 10:e36310. [PMID: 39253122 PMCID: PMC11381786 DOI: 10.1016/j.heliyon.2024.e36310] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/04/2024] [Revised: 08/06/2024] [Accepted: 08/13/2024] [Indexed: 09/11/2024] Open
Abstract
Background and rationale Febrile neutropenia (FN) is one of the major causes of early mortality among children undergoing induction chemotherapy for haematological malignancies. FN occurs in up to 80 % of the children undergoing intensive chemotherapy and FN specific mortality is as high as 10 %. The management of high-risk FN (HR-FN) is by early initiation of broad-spectrum empirical antibiotic therapy (EAT) which is continued till blood count recovery. Adverse effects of prolonged EAT among children without proven infective focus have questioned the rationale behind the duration of EAT. The non inferiority of early stoppage of EAT in patients with low-risk FN (LR-FN) when afebrile for 48 h, irrespective of marrow recovery, is proven among adults and children. However, there is paucity of data regarding the same in children with HR-FN. This study aims to determine whether early discontinuation of EAT in children with HR-FN without proven infective focus who become afebrile and awaiting marrow recovery, would reduce antibiotic duration and their adverse effects without any negative consequences for patients. Objective To compare the rates of recurrent fever in paediatric patients (2-18 years) with HR-FN when EAT is continued till marrow recovery (control group) versus when stopped early at defervescence irrespective of marrow recovery (study group). Methodology This is the study protocol of a phase 3, single centre, randomized, open label, non-inferiority clinical trial. The primary outcome is the rate of fever recurrence among patients with HR-FN, when EAT is stopped early irrespective of marrow recovery (study group) and will be compared to the rate of fever recurrence on continuation of EAT till marrow recovery which is defined as an absolute neutrophil count (ANC) ≥ 500/mm3 (control group). Secondary outcomes include the comparison of duration of antibiotic use, mortality rates, hospital re-admission rates, requirement of multiple broad-spectrum antibiotics, therapeutic anti-fungal usage and need for organ support between the study and the control groups. A total of 280 children with acute leukaemia undergoing EAT for grade 3 or severe FN (ANC <500/μL) without clinico-laboratory evidence of infective foci are being randomized in the ratio of 1:1 between the study and the control group after defervescence for 48 h. The patients will be followed up for primary outcome (fever recurrence) till the end of induction period (day 35) or recovery of ANC ≥500/mm3 whichever is earlier. Expected outcome ESAT-HR FN study is the first large phase 3 randomised study to assess the impact of early stoppage of EAT irrespective of marrow recovery among a homogenous paediatric cohort of HR-FN in the setting of induction chemotherapy for acute leukaemia. This study will be seminal in addressing the duration of EAT in HR-FN among children without infective foci and if proven to be non-inferior this strategy will help to reduce the adverse effects from prolonged antibiotic use, the emergence of drug resistance, decrease hospital stay length and overall health care costs.
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Affiliation(s)
- Santhosh Kumar Kn
- Department of Medical Oncology, Dr. Bhimrao Ambedkar Institute Rotary Cancer Hospital, All India Institute of Medical Sciences, New Delhi, India
| | - Santhosh Kumar Chellapuram
- Department of Medical Oncology, Dr. Bhimrao Ambedkar Institute Rotary Cancer Hospital, All India Institute of Medical Sciences, New Delhi, India
| | - Shuvadeep Ganguly
- Department of Medical Oncology, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Puducherry, India
| | - Deepam Pushpam
- Department of Medical Oncology, Dr. Bhimrao Ambedkar Institute Rotary Cancer Hospital, All India Institute of Medical Sciences, New Delhi, India
| | - Rupak Kumar Giri
- Department of Medical Oncology, Dr. Bhimrao Ambedkar Institute Rotary Cancer Hospital, All India Institute of Medical Sciences, New Delhi, India
| | - Sameer Bakhshi
- Department of Medical Oncology, Dr. Bhimrao Ambedkar Institute Rotary Cancer Hospital, All India Institute of Medical Sciences, New Delhi, India
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Ferreira NE, da Costa AC, Kallas EG, Silveira CGT, de Oliveira ACS, Honorato L, Paião HGO, Lima SH, de M. Vasconcelos D, Côrtes MF, Costa SF, Mendoza TRT, Gomes HR, Witkin SS, Mendes-Correa MC. Encephalopathy Caused by Human Parvovirus B19 Genotype 1 Associated with Haemophilus influenzae Meningitis in a Newborn. Curr Issues Mol Biol 2023; 45:6958-6966. [PMID: 37754223 PMCID: PMC10529629 DOI: 10.3390/cimb45090439] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/09/2023] [Revised: 07/12/2023] [Accepted: 07/15/2023] [Indexed: 09/28/2023] Open
Abstract
Parvovirus B19 infection is associated with a wide range of clinical manifestations, from asymptomatic to severe neurological disorders. Its major clinical symptoms, fever and rash, are common to multiple viruses, and laboratory tests to detect B19 are frequently not available. Thus, the impact of B19 on public health remains unclear. We report the case of a 38-day old girl admitted to São Paulo Clinical Hospital, Brazil, with an initial diagnosis of bacterial meningitis, seizures, and acute hydrocephalus. Antibiotic therapy was maintained for one week after admission and discontinued after negative laboratory results were obtained. Nine days after symptoms onset, a cerebral spinal fluid (CSF) sample revealed persistent pleocytosis. The complete B19 complete genome was subsequently identified in her CSF by a metagenomic next-generation sequencing approach. This report highlights the possible involvement of B19 in the occurrence of acute neurological manifestations and emphasizes that its possible involvement might be better revealed by the use of metagenomic technology to detect viral agents in clinical situations of unknown or uncertain etiology.
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Affiliation(s)
- Noely Evangelista Ferreira
- Departamento de Molestias Infecciosas e Parasitarias, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05403-000, Brazil; (N.E.F.); (A.C.d.C.); (E.G.K.); (L.H.); (H.G.O.P.); (S.H.L.); (M.F.C.); (S.F.C.); (T.R.T.M.)
- Instituto de Medicina Tropical, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05403-000, Brazil; (D.d.M.V.); (S.S.W.)
| | - Antonio C. da Costa
- Departamento de Molestias Infecciosas e Parasitarias, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05403-000, Brazil; (N.E.F.); (A.C.d.C.); (E.G.K.); (L.H.); (H.G.O.P.); (S.H.L.); (M.F.C.); (S.F.C.); (T.R.T.M.)
- Instituto de Medicina Tropical, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05403-000, Brazil; (D.d.M.V.); (S.S.W.)
| | - Esper G. Kallas
- Departamento de Molestias Infecciosas e Parasitarias, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05403-000, Brazil; (N.E.F.); (A.C.d.C.); (E.G.K.); (L.H.); (H.G.O.P.); (S.H.L.); (M.F.C.); (S.F.C.); (T.R.T.M.)
| | - Cassia G. T. Silveira
- Division of Clinical Immunology and Allergy, School of Medicine, University of São Paulo, São Paulo 05403-000, Brazil; (C.G.T.S.); (A.C.S.d.O.)
| | - Ana Carolina S. de Oliveira
- Division of Clinical Immunology and Allergy, School of Medicine, University of São Paulo, São Paulo 05403-000, Brazil; (C.G.T.S.); (A.C.S.d.O.)
| | - Layla Honorato
- Departamento de Molestias Infecciosas e Parasitarias, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05403-000, Brazil; (N.E.F.); (A.C.d.C.); (E.G.K.); (L.H.); (H.G.O.P.); (S.H.L.); (M.F.C.); (S.F.C.); (T.R.T.M.)
- Instituto de Medicina Tropical, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05403-000, Brazil; (D.d.M.V.); (S.S.W.)
| | - Heuder G. O. Paião
- Departamento de Molestias Infecciosas e Parasitarias, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05403-000, Brazil; (N.E.F.); (A.C.d.C.); (E.G.K.); (L.H.); (H.G.O.P.); (S.H.L.); (M.F.C.); (S.F.C.); (T.R.T.M.)
- Instituto de Medicina Tropical, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05403-000, Brazil; (D.d.M.V.); (S.S.W.)
| | - Silvia H. Lima
- Departamento de Molestias Infecciosas e Parasitarias, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05403-000, Brazil; (N.E.F.); (A.C.d.C.); (E.G.K.); (L.H.); (H.G.O.P.); (S.H.L.); (M.F.C.); (S.F.C.); (T.R.T.M.)
- Instituto de Medicina Tropical, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05403-000, Brazil; (D.d.M.V.); (S.S.W.)
| | - Dewton de M. Vasconcelos
- Instituto de Medicina Tropical, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05403-000, Brazil; (D.d.M.V.); (S.S.W.)
| | - Marina F. Côrtes
- Departamento de Molestias Infecciosas e Parasitarias, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05403-000, Brazil; (N.E.F.); (A.C.d.C.); (E.G.K.); (L.H.); (H.G.O.P.); (S.H.L.); (M.F.C.); (S.F.C.); (T.R.T.M.)
- Instituto de Medicina Tropical, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05403-000, Brazil; (D.d.M.V.); (S.S.W.)
| | - Silvia F. Costa
- Departamento de Molestias Infecciosas e Parasitarias, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05403-000, Brazil; (N.E.F.); (A.C.d.C.); (E.G.K.); (L.H.); (H.G.O.P.); (S.H.L.); (M.F.C.); (S.F.C.); (T.R.T.M.)
- Instituto de Medicina Tropical, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05403-000, Brazil; (D.d.M.V.); (S.S.W.)
| | - Tania R. T. Mendoza
- Departamento de Molestias Infecciosas e Parasitarias, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05403-000, Brazil; (N.E.F.); (A.C.d.C.); (E.G.K.); (L.H.); (H.G.O.P.); (S.H.L.); (M.F.C.); (S.F.C.); (T.R.T.M.)
- Instituto de Medicina Tropical, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05403-000, Brazil; (D.d.M.V.); (S.S.W.)
| | - Hélio R. Gomes
- Laboratório de Investigação Médica LIM 15, Hospital da Clinicas da, Faculdade de Medicina da, Universidade de São Paulo, São Paulo 01246-903, Brazil;
| | - Steven S. Witkin
- Instituto de Medicina Tropical, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05403-000, Brazil; (D.d.M.V.); (S.S.W.)
- Department of Obstetrics and Gynecology, Weill Cornell Medicine, 1300 York Avenue, New York, NY 10065, USA
| | - Maria C. Mendes-Correa
- Departamento de Molestias Infecciosas e Parasitarias, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05403-000, Brazil; (N.E.F.); (A.C.d.C.); (E.G.K.); (L.H.); (H.G.O.P.); (S.H.L.); (M.F.C.); (S.F.C.); (T.R.T.M.)
- Instituto de Medicina Tropical, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05403-000, Brazil; (D.d.M.V.); (S.S.W.)
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Monteiro VS, Baía-da-Silva DC, Silva VA, Pivoto João GA, Marinho EPM, Cubas-Vega NC, Val FFA, Perez-Gomez AS, Monte RL, Mota A, Lacerda MVG, Souza Bastos M. Neurological Manifestations Associated with Parvovirus B19 Infection in Immunocompetent Children: Case Series and Systematic Review. J Trop Pediatr 2021; 67:fmab078. [PMID: 34545404 DOI: 10.1093/tropej/fmab078] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/14/2022]
Abstract
An increasing number of reports have described human parvovirus B19 infection in association with a variety of neurological manifestations, especially in children. This study assessed the clinical and laboratory outcomes found in a case series of immunocompetent children who tested positive for parvovirus B19 by qualitative polymerase chain reaction assays of cerebrospinal fluid, in a tertiary referral center in the western Brazilian Amazon. We screened 178 children with clinically diagnosed central nervous system infections (meningoencephalitis). Of these, five (2.8%) were positive for parvovirus B19. A literature review also presented herein identified a further 50 cases of parvovirus B19 with neurological manifestations. Thus, even if the classic signs of parvovirus B19 infection are absent, such as the well-known rash, children with signs of neurological infection should also be evaluated for parvovirus B19 infection.
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Affiliation(s)
- Vinícius Silva Monteiro
- Instituto de Pesquisa Clínica Carlos Borborema, Fundação de Medicina Tropical Dr Heitor Vieira Dourado, Manaus, Amazonas 69040-000, Brazil
| | - Djane Clarys Baía-da-Silva
- Instituto de Pesquisa Clínica Carlos Borborema, Fundação de Medicina Tropical Dr Heitor Vieira Dourado, Manaus, Amazonas 69040-000, Brazil
- Programa de Pós-Graduação em Medicina Tropical, Universidade do Estado do Amazonas, Manaus 69040-000, Brazil
- Instituto Leônidas and Maria Deane, Fiocruz, Manaus 69.057-070, Brazil
| | - Valderjane Aprigio Silva
- Instituto de Pesquisa Clínica Carlos Borborema, Fundação de Medicina Tropical Dr Heitor Vieira Dourado, Manaus, Amazonas 69040-000, Brazil
| | - Guilherme Augusto Pivoto João
- Instituto de Pesquisa Clínica Carlos Borborema, Fundação de Medicina Tropical Dr Heitor Vieira Dourado, Manaus, Amazonas 69040-000, Brazil
| | - Eveny Perlize Melo Marinho
- Programa de Pós-Graduação em Ciências da Saúde, Universidade Federal do Amazonas, Manaus 69077-000, Brazil
| | - Nadia Carolina Cubas-Vega
- Programa de Pós-Graduação em Medicina Tropical, Universidade do Estado do Amazonas, Manaus 69040-000, Brazil
| | - Fernando Fonseca Almeida Val
- Instituto de Pesquisa Clínica Carlos Borborema, Fundação de Medicina Tropical Dr Heitor Vieira Dourado, Manaus, Amazonas 69040-000, Brazil
- Programa de Pós-Graduação em Medicina Tropical, Universidade do Estado do Amazonas, Manaus 69040-000, Brazil
| | - Aline Stephanie Perez-Gomez
- Instituto de Pesquisa Clínica Carlos Borborema, Fundação de Medicina Tropical Dr Heitor Vieira Dourado, Manaus, Amazonas 69040-000, Brazil
| | - Rossiclea Lins Monte
- Instituto de Pesquisa Clínica Carlos Borborema, Fundação de Medicina Tropical Dr Heitor Vieira Dourado, Manaus, Amazonas 69040-000, Brazil
| | - Adolfo Mota
- Programa de Pós-Graduação em Ciências da Saúde, Universidade Federal do Amazonas, Manaus 69077-000, Brazil
| | - Marcus Vinícius Guimarães Lacerda
- Instituto de Pesquisa Clínica Carlos Borborema, Fundação de Medicina Tropical Dr Heitor Vieira Dourado, Manaus, Amazonas 69040-000, Brazil
- Programa de Pós-Graduação em Medicina Tropical, Universidade do Estado do Amazonas, Manaus 69040-000, Brazil
| | - Michele Souza Bastos
- Instituto de Pesquisa Clínica Carlos Borborema, Fundação de Medicina Tropical Dr Heitor Vieira Dourado, Manaus, Amazonas 69040-000, Brazil
- Programa de Pós-Graduação em Ciências da Saúde, Universidade Federal do Amazonas, Manaus 69077-000, Brazil
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Alawadhi A, Saint-Martin C, Bhanji F, Srour M, Atkinson J, Sébire G. Acute Hemorrhagic Encephalitis Responding to Combined Decompressive Craniectomy, Intravenous Immunoglobulin, and Corticosteroid Therapies: Association with Novel RANBP2 Variant. Front Neurol 2018; 9:130. [PMID: 29593631 PMCID: PMC5857578 DOI: 10.3389/fneur.2018.00130] [Citation(s) in RCA: 8] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/09/2017] [Accepted: 02/21/2018] [Indexed: 11/21/2022] Open
Abstract
Background Acute hemorrhagic encephalomyelitis (AHEM) is considered as a rare form of acute disseminated encephalomyelitis characterized by fulminant encephalopathy with hemorrhagic necrosis and most often fatal outcome. Objective To report the association with Ran Binding Protein (RANBP2) gene variant and the response to decompressive craniectomy and high-dose intravenous methylprednisolone (IVMP) in life-threatening AHEM. Design Single case study. Case report A 6-year-old girl known to have sickle cell disease (SCD) presented an acquired demyelinating syndrome (ADS) with diplopia due to sudden unilateral fourth nerve palsy. She received five pulses of IVMP (30 mg/kg/day). Two weeks after steroid weaning, she developed right hemiplegia and coma. Brain magnetic resonance imaging showed a left frontal necrotico-hemorrhagic lesion and new multifocal areas of demyelination. She underwent decompressive craniotomy and evacuation of an ongoing left frontoparietal hemorrhage. Comprehensive investigations ruled out vascular and infectious process. The neurological deterioration stopped concomitantly with combined neurosurgical drainage of the hematoma, decompressive craniotomy, IVMP, and intravenous immunoglobulins (IVIG). She developed during the following months Crohn disease and sclerosing cholangitis. After 2-year follow-up, there was no new neurological manifestation. The patient still suffered right hemiplegia and aphasia, but was able to walk. Cognitive/behavioral abilities significantly recovered. A heterozygous novel rare missense variant (c.4993A>G, p.Lys1665Glu) was identified in RANBP2, a gene associated with acute necrotizing encephalopathy. RANBP2 is a protein playing an important role in the energy homeostasis of neuronal cells. Conclusion In any ADS occurring in the context of SCD and/or autoimmune condition, we recommend to slowly wean steroids and to closely monitor the patient after weaning to quickly treat any recurrence of neurological symptom with IVMP. This case report, in addition to others, stresses the likely efficacy of combined craniotomy, IVIG, and IVMP treatments in AHEM. RANBP2 mutations may sensitize the brain to inflammation and predispose to AHEM.
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Affiliation(s)
- Abdulla Alawadhi
- Division of Pediatric Neurology, Department of Pediatrics, Montreal Children's Hospital, Montreal, QC, Canada
| | - Christine Saint-Martin
- Department of Medical Imaging, Montreal Children's Hospital, McGill University, Montreal, QC, Canada
| | - Farhan Bhanji
- Pediatric Intensive Care Unit, Department of Pediatrics, Montreal Children's Hospital, McGill University, Montreal, QC, Canada
| | - Myriam Srour
- Division of Pediatric Neurology, Department of Pediatrics, Montreal Children's Hospital, Montreal, QC, Canada
| | - Jeffrey Atkinson
- Division of Neurosurgery, Department of Surgery, Montreal Children's Hospital, McGill University, Montreal, QC, Canada
| | - Guillaume Sébire
- Division of Pediatric Neurology, Department of Pediatrics, Montreal Children's Hospital, Montreal, QC, Canada
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Abstract
Parvovirus B19 (B19V) and human bocavirus 1 (HBoV1), members of the large Parvoviridae family, are human pathogens responsible for a variety of diseases. For B19V in particular, host features determine disease manifestations. These viruses are prevalent worldwide and are culturable in vitro, and serological and molecular assays are available but require careful interpretation of results. Additional human parvoviruses, including HBoV2 to -4, human parvovirus 4 (PARV4), and human bufavirus (BuV) are also reviewed. The full spectrum of parvovirus disease in humans has yet to be established. Candidate recombinant B19V vaccines have been developed but may not be commercially feasible. We review relevant features of the molecular and cellular biology of these viruses, and the human immune response that they elicit, which have allowed a deep understanding of pathophysiology.
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Affiliation(s)
- Jianming Qiu
- Department of Microbiology, Molecular Genetics and Immunology, University of Kansas Medical Center, Kansas City, Kansas, USA
| | | | - Neal S Young
- Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA
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Abstract
ABSTRACT
Primary parvovirus B19 infection is an infrequent, but serious and treatable, cause of chronic anemia in immunocompromised hosts. Many compromised hosts have preexisting antibody to B19 and are not at risk. However, upon primary infection, some patients may be able to mount a sufficient immune response to terminate active parvovirus B19 infection of erythroid precursors. The most common consequence of B19 infection in the compromised host is pure red-cell aplasia, resulting in chronic or recurrent anemia with reticulocytopenia. Anemia persists until neutralizing antibody is either produced by the host or passively administered. Parvovirus B19 should be suspected in compromised hosts with unexplained or severe anemia and reticulocytopenia, or when bone-marrow examination shows either giant pronormoblasts or absence of red-cell precursors. Diagnosis is established by detection of B19 DNA in serum in the absence of IgG antibody to B19. In some cases, IgG antibody is detected but is not neutralizing. Anti-B19 IgM may or may not be present. Therapy includes any or all of the following: red-cell transfusion, adjustment in medications to restore or improve the patient’s immune system, and administration of intravenous immunoglobulin (IVIG). Following treatment, patients should be closely monitored, especially if immunosuppression is unchanged or increased. Should hematocrit trend downward and parvovirus DNA trend upward, the therapeutic options above should be revisited. In a few instances, monthly maintenance IVIG may be indicated. Caregivers should be aware that B19 variants, though rarely encountered, can be missed or under-quantitated by some real-time polymerase-chain reaction methods.
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Watanabe T, Kawashima H. Acute encephalitis and encephalopathy associated with human parvovirus B19 infection in children. World J Clin Pediatr 2015; 4:126-134. [PMID: 26566485 PMCID: PMC4637803 DOI: 10.5409/wjcp.v4.i4.126] [Citation(s) in RCA: 19] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/24/2015] [Revised: 08/11/2015] [Accepted: 09/10/2015] [Indexed: 02/06/2023] Open
Abstract
Reports of neurologic manifestations of human parvovirus B19 (B19) infection have been on the rise. Acute encephalitis and encephalopathy is the most common, accounting for 38.8% of total B19-associated neurological manifestations. To date, 34 children with B19 encephalitis and encephalopathy have been reported, which includes 21 encephalitis and 13 encephalopathy cases. Ten (29%) were immunocompromised and 17 (39%) had underlying diseases. Fever at the onset of disease and rash presented in 44.1% and 20.6% of patients, respectively. Neurological manifestations include alteration of consciousness occurred in all patients, seizures in 15 (44.1%) patients, and focal neurologic signs in 12 (35.3%) patients. Anemia and pleocytosis in cerebrospinal fluid (CSF) occurred in 56.3% and 48.1% of patients, respectively. Serum Anti-B19 IgM (82.6%) and CSF B19 DNA (90%) were positive in the majority of cases. Some patients were treated with intravenous immunoglobulins and/or steroids, although an accurate evaluation of the efficacy of these treatment modalities cannot be determined. Nineteen (57.6%) patients recovered completely, 11 (33.3%) patients had some neurological sequelae and 3 (8.8%) patients died. Although the precise pathogenesis underlying the development of B19 encephalitis and encephalopathy is unclear, direct B19 infection or NS1protein of B19 toxicity in the brain, and immune-mediated brain injuries have been proposed.
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Suzuki M, Yoto Y, Ishikawa A, Asakura H, Tsutsumi H. Acute transverse myelitis associated with human parvovirus b19 infection. J Child Neurol 2014; 29:280-2. [PMID: 24049056 DOI: 10.1177/0883073813499824] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/16/2022]
Abstract
We describe severe acute transverse myelitis in a previously healthy 9-year-old boy in whom primary human parvovirus B19 infection was confirmed serologically and B19 DNA was detected in his serum and cerebrospinal fluid. Besides erythema infectiosum, parvovirus B19 infection has various clinical manifestations; however, central nervous system involvement is rare. Even more unusual is parvovirus B19-associated acute transverse myelitis.
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Affiliation(s)
- Masashi Suzuki
- 1Department of Pediatrics, Sapporo Medical University School of Medicine, Sapporo, Japan
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Barah F, Whiteside S, Batista S, Morris J. Neurological aspects of human parvovirus B19 infection: a systematic review. Rev Med Virol 2014; 24:154-68. [PMID: 24459081 PMCID: PMC4238837 DOI: 10.1002/rmv.1782] [Citation(s) in RCA: 66] [Impact Index Per Article: 6.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/22/2013] [Revised: 11/28/2013] [Accepted: 11/29/2013] [Indexed: 02/06/2023]
Abstract
Parvovirus B19 has been linked with various clinical syndromes including neurological manifestations. However, its role in the latter remains not completely understood. Although the last 10 years witnessed a surge of case reports on B19-associated neurological aspects, the literature data remains scattered and heterogeneous, and epidemiological information on the incidence of B19-associated neurological aspects cannot be accurately extrapolated. The aim of this review is to identify the characteristics of cases of B19-associated neurological manifestations. A computerized systematic review of existing literature concerning cases of B19-related neurological aspects revealed 89 articles describing 129 patients; 79 (61.2%) were associated with CNS manifestations, 41 (31.8%) were associated with peripheral nervous system manifestations, and 9 (7.0%) were linked with myalgic encephalomyelitis. The majority of the cases (50/129) had encephalitis. Clinical characteristic features of these cases were analyzed, and possible pathological mechanisms were also described. In conclusion, B19 should be included in differential diagnosis of encephalitic syndromes of unknown etiology in all age groups. Diagnosis should rely on investigation of anti-B19 IgM antibodies and detection of B19 DNA in serum or CSF. Treatment of severe cases might benefit from a combined regime of intravenous immunoglobulins and steroids. To confirm these outcomes, goal-targeted studies are recommended to exactly identify epidemiological scenarios and explore potential pathogenic mechanisms of these complications. Performing retrospective and prospective and multicenter studies concerning B19 and neurological aspects in general, and B19 and encephalitic syndromes in particular, are required. © 2014 The Authors. Reviews in Medical Virology published by John Wiley & Sons, Ltd.
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Affiliation(s)
- Faraj Barah
- Center for Neuroscience and Cell Biology, Faculty of Medicine, University of Coimbra, Coimbra, Portugal
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Slavov SN, Kashima S, Silva-Pinto AC, Amarilla AA, Aquino VH, Covas DT. Molecular and clinical evaluation of the acute human parvovirus B19 infection: comparison of two cases in children with sickle cell disease and discussion of the literature. Braz J Infect Dis 2013; 17:97-101. [PMID: 23290473 PMCID: PMC9427394 DOI: 10.1016/j.bjid.2012.06.026] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/20/2012] [Revised: 05/04/2012] [Accepted: 06/02/2012] [Indexed: 10/29/2022] Open
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12
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Benseler S, Pohl D. Childhood central nervous system vasculitis. HANDBOOK OF CLINICAL NEUROLOGY 2013; 112:1065-78. [DOI: 10.1016/b978-0-444-52910-7.00024-6] [Citation(s) in RCA: 19] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/04/2022]
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13
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Ballas SK, Kesen MR, Goldberg MF, Lutty GA, Dampier C, Osunkwo I, Wang WC, Hoppe C, Hagar W, Darbari DS, Malik P. Beyond the definitions of the phenotypic complications of sickle cell disease: an update on management. ScientificWorldJournal 2012; 2012:949535. [PMID: 22924029 PMCID: PMC3415156 DOI: 10.1100/2012/949535] [Citation(s) in RCA: 98] [Impact Index Per Article: 7.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/13/2012] [Accepted: 04/01/2012] [Indexed: 12/25/2022] Open
Abstract
The sickle hemoglobin is an abnormal hemoglobin due to point mutation (GAG → GTG) in exon 1 of the β globin gene resulting in the substitution of glutamic acid by valine at position 6 of the β globin polypeptide chain. Although the molecular lesion is a single-point mutation, the sickle gene is pleiotropic in nature causing multiple phenotypic expressions that constitute the various complications of sickle cell disease in general and sickle cell anemia in particular. The disease itself is chronic in nature but many of its complications are acute such as the recurrent acute painful crises (its hallmark), acute chest syndrome, and priapism. These complications vary considerably among patients, in the same patient with time, among countries and with age and sex. To date, there is no well-established consensus among providers on the management of the complications of sickle cell disease due in part to lack of evidence and in part to differences in the experience of providers. It is the aim of this paper to review available current approaches to manage the major complications of sickle cell disease. We hope that this will establish another preliminary forum among providers that may eventually lead the way to better outcomes.
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Affiliation(s)
- Samir K Ballas
- Cardeza Foundation and Department of Medicine, Thomas Jefferson University, 1015 Walnut Street, Philadelphia, PA 19107, USA.
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Slavov SN, Kashima S, Pinto ACS, Covas DT. Human parvovirus B19: general considerations and impact on patients with sickle-cell disease and thalassemia and on blood transfusions. ACTA ACUST UNITED AC 2011; 62:247-62. [DOI: 10.1111/j.1574-695x.2011.00819.x] [Citation(s) in RCA: 41] [Impact Index Per Article: 2.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/16/2022]
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Grant JK, Yin NC, Zaytoun AM, Waseem H, Hobbs JA. Persistent adeno-associated virus 2 and parvovirus B19 sequences in post-mortem human cerebellum. THE CEREBELLUM 2009; 8:490-8. [PMID: 19585179 DOI: 10.1007/s12311-009-0126-4] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Subscribe] [Scholar Register] [Received: 03/19/2009] [Accepted: 06/24/2009] [Indexed: 12/18/2022]
Abstract
We previously reported in a large cohort (N = 104) of post-mortem tissues the detection of both the non-pathogenic adeno-associated virus (AAV2) in approximately 13% and the pathogenic human parvovirus B19 (B19) in approximately 42% of human brains, particularly the dorsolateral prefrontal cortex. Multiple animal parvoviruses target the developing cerebellum (CBLM) resulting in hypoplasia and ataxia, but very little is known about the human parvoviruses and their ability to infect or cause disease in the CBLM. We have now confirmed in the above cohort the presence of AAV2 and B19 sequences in the CBLM. Our results show that approximately 27% and approximately 70% of human CBLM are positive by nested polymerase chain reaction for AAV2 and B19 sequences, respectively. We also document in a second cohort (N = 10) the presence of AAV2 (50%) and B19 (100%) sequences in the CBLM and correlate our results for B19 with studies from matched sera. Eighty percent (80%) of this cohort was positive for anti-B19 IgG, while none were IgM+, suggesting that most individuals had been previously infected with B19 but none acutely. To our knowledge, this study is the first to demonstrate that both AAV2 and B19 sequences are present at relatively high frequencies in the CBLM and are likely due to persistent rather than acute infection. Further studies will lead to insights into AAV2- and/or B19-CBLM interactions including mechanisms of infection, persistence, and possibly neuropathology, including cerebellar hypoplasia and ataxia.
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Affiliation(s)
- James K Grant
- Department of Psychiatry, University of Florida College of Medicine, Gainesville, FL 32610, USA
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Abstract
A 9-year-old girl with hereditary spherocytosis developed aplastic crisis and encephalopathy associated with human parvovirus B19 (PVB19) infection. During the clinical course, we followed PVB19 DNA in her plasma and cerebrospinal fluid by real-time polymerase chain reaction and found that her symptoms of encephalopathy had occurred at the peak viral load. PVB19-associated encephalopathy might occur as a result of direct invasion by PVB19.
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Krishnamurti L, Lanford L, Munoz R. Life threatening parvovirus B19 and herpes simplex virus associated acute myocardial dysfunction in a child with homozygous sickle cell disease. Pediatr Blood Cancer 2007; 49:1019-21. [PMID: 16700044 DOI: 10.1002/pbc.20855] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/12/2022]
Abstract
Human parvovirus (HPV) B19, a common infection, frequently causes transient red cell aplasia in children with hemolytic anemia, such as sickle cell disease (SCD). It was considered to be a self-limited condition, easily treated with blood transfusion. However, acute splenic sequestration, acute chest syndrome, nephrotic syndrome, and stroke have been reported in SCD patients following HPV B19 infection. We report a 3-year-old child with SCD who developed fulminant myocarditis following HPV B19-related aplastic crisis. The diagnosis of myocarditis should be considered in a patient with hemolytic anemia with an infection with HPV B19 who develops signs of cardiopulmonary failure despite correction of anemia.
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Affiliation(s)
- Lakshmanan Krishnamurti
- Division of Hematology/Oncology/BMT, Children's Hospital of Pittsburgh, University of Pittsburgh Medical Center Health System, Pittsburgh, Pennsylvania 15213, USA.
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Kirkham FJ. Therapy Insight: stroke risk and its management in patients with sickle cell disease. ACTA ACUST UNITED AC 2007; 3:264-78. [PMID: 17479074 DOI: 10.1038/ncpneuro0495] [Citation(s) in RCA: 47] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/14/2006] [Accepted: 03/15/2007] [Indexed: 11/09/2022]
Abstract
Children with sickle cell disease, a chronic hemolytic anemia, present with a wide variety of neurological syndromes, including ischemic and hemorrhagic stroke, transient ischemic attacks, 'soft neurological signs', seizures, headache, coma, visual loss, altered mental status, cognitive difficulties, and covert or 'silent' infarction. Those with ischemic stroke usually have stenosis or occlusion of the distal internal carotid and proximal middle cerebral arteries. Indefinite transfusion prevents recurrence in most patients who have had a stroke, and can prevent first stroke in those with high transcranial Doppler velocities. High white cell count, low hemoglobin and oxyhemoglobin desaturation predict neurological complications. Other risk factors for overt ischemic stroke include hypertension, previous transient ischemic attack, covert infarction and chest crisis. For hemorrhagic stroke, aneurysms are common in adults but not children, who often present with hypertension after transfusion or corticosteroids. Seizures are particularly common in patients with cerebrovascular disease and covert infarction; the latter is also associated with hyposplenism and infrequent pain. Factors associated with cognitive difficulties include thrombocytosis, infarction, large-vessel disease, and perfusion abnormality on neuroimaging. As well as investigating the role of genes and the possibility that hydroxyurea or blood pressure control reduce neurological complications, we should explore the modifiable effects of poor nutrition, chronic infection, hemolysis and oxyhemoglobin desaturation on stroke risk.
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Affiliation(s)
- Fenella J Kirkham
- Neurosciences Unit, University College London Institute of Child Health, London, UK.
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Wang WC. Central Nervous System Complications of Sickle Cell Disease in Children: An Overview. Child Neuropsychol 2007; 13:103-19. [PMID: 17364568 DOI: 10.1080/09297040600788136] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/24/2022]
Abstract
Complications involving the central nervous system are among the most devastating manifestations of sickle cell disease. Although overt stroke occurs in 1 in 10 children with Hemoglobin SS, "silent cerebral infarcts" are even more frequent. Both are associated with significant neuropsychological deficits. The end result of these effects on the CNS often is diminished school performance. The use of transcranial Doppler ultrasonography screening allows the identification of patients at high risk for clinical stroke as well as stroke prevention by chronic transfusion. However, definitive prophylaxis and treatment for most CNS complications of sickle cell disease have yet to be determined.
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Affiliation(s)
- Winfred C Wang
- Department of Hematology/Oncology, St. Jude Children's Research Hospital. Memphis, TN38105, USA.
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Hobbs JA. Detection of adeno-associated virus 2 and parvovirus B19 in the human dorsolateral prefrontal cortex. J Neurovirol 2006; 12:190-9. [PMID: 16877300 DOI: 10.1080/13550280600827351] [Citation(s) in RCA: 27] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
Although animal parvoviruses have long been recognized as causes of brain pathology in multiple animal models, especially during early development, human parvoviruses are rarely thought of as neurotropic or causes of neuropathology in humans. However, several recent case reports have suggested possible associations of parvovirus B19 (B19) infection with various neurological and neuropsychiatric symptoms. Adeno-associated virus 2 (AAV2) is related to B19 but has thus far not been shown to be associated with any human disease but is of clinical interest because of the recent use of recombinant AAV vectors in human gene therapy, including gene delivery to the brain. To date, there have been no large-scale studies of the propensity of wild-type human parvoviruses to infect the brain. The Stanley Medical Research Institute Brain Collection offered a unique opportunity to study a large sample (n = 104) of dorsolateral prefrontal cortex (DLPC) DNAs isolated from unaffected control, schizophrenic, and bipolar disorder brains for the presence of parvoviral sequences. This is the first investigator-blinded study to document the presence of parvoviral sequences in the DLPC by utilizing highly sensitive nested polymerase chain reaction (nPCR) and DNA sequencing. Of the overall sample, 6.7% to 12.5% were positive for AAV2, and 14.4% to 42.3% were positive for B19 sequences, with no statistical differences among subgroups. This is the first report to demonstrate the presence of human parvoviruses in a large cohort of adult DLPC, which underscores the need to gain a better insight into the basic biology of parvovirus-brain interactions, including mechanisms of infection and persistence.
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Affiliation(s)
- Jacqueline A Hobbs
- Department of Psychiatry and the Evelyn F. and William L. McKnight Brain Institute, University of Florida College of Medicine, Gainesville, Florida 32610, USA.
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Schröder C, Pfeiffer S, Wu G, Azimzadeh AM, Aber A, Pierson RN, O'Sullivan MG. Simian parvovirus infection in cynomolgus monkey heart transplant recipients causes death related to severe anemia. Transplantation 2006; 81:1165-70. [PMID: 16641603 DOI: 10.1097/01.tp.0000203170.77195.e4] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/26/2022]
Abstract
BACKGROUND Simian parvovirus (SPV) was first isolated from cynomolgus monkeys. Like human parvovirus B19, this virus has a predilection for erythroid cells. During acute SPV infection, clinical signs are usually mild or inapparent, but severe anemia may occur in immunocompromised animals. We report several cases of symptomatic SPV infection in cynomolgus monkeys following heart transplantation. METHODS Twenty-three consecutive abdominal heterotopic heart transplants were studied. Viremia, measured by dot blot and/or PCR, and SPV-specific antibodies were determined retrospectively. RESULTS All except one animal were on an immunosuppressive protocol. In all, 48% (11/23) of transplant recipients had viremia with SPV detected at some point after transplant. An additional 22% seroconverted before or after transplant, and were asymptomatic without detectable SPV. Of the 11 acutely viremic animals, five were euthanized because of severe anemia attributed to SPV. The remaining 30% of the transplant recipients did not seroconvert and were asymptomatic. Of seven recipients of donor tissue from seropositive or viremic animals, five became viremic and three died with anemia. No immunosuppressive regimen was implicated in increased susceptibility; the one transplant recipient not treated with immunosuppressive agents died with anemia and acute viremia two weeks after explant of a rejected graft. CONCLUSION SPV is an important pathogen in surgically manipulated cynomolgus monkeys, particularly with immune compromise. Once introduced into a colony, clinically silent SPV infection could be readily transmitted within the environment. Transmission and disease occur at high frequency with an organ from a PCR-negative, seropositive donor, suggesting that latent virus can be conveyed by the organ.
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Affiliation(s)
- Carsten Schröder
- Division of Cardiac Surgery, University of Maryland, Baltimore, MD 21201, USA
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Abstract
PURPOSE OF REVIEW In recent years, many investigators have focused on potential associations between infections and vascular inflammation. We review the principal pathogenic mechanisms that have been implicated for possible roles in the vascular inflammation initiated by infectious agents. We also summarize the most important literature related to this topic. RECENT FINDINGS A novel theory known as autoantigen complementarity suggests that an infectious agent could trigger antineutrophil cytoplasmic antibody-associated vasculitis. Several recent studies investigating the presence of parvovirus B19 and herpesviruses in temporal arteries with giant cell arteritis have yielded contradictory results. A recent study has identified higher frequency of a novel human virus, the 'New Haven coronavirus', in respiratory secretions of children with Kawasaki disease. Many case reports have suggested potential relationships between human pathogens and vasculitis. SUMMARY There remains considerable interest in the possibilities of primary vasculitic syndromes caused in some fashion by infection. With the exception of a few well sustained associations - for example hepatitis B or C with known vasculitic syndromes - most of the purported links between microbial agents and primary vasculitides remain speculative.
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Affiliation(s)
- Alicia Rodríguez-Pla
- Division of Molecular and Clinical Rheumatology, The Johns Hopkins School of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21224, USA
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Affiliation(s)
- Toru Watanabe
- Department of Paediatrics, Niigata City General Hospital, 2-6-1 Shichikuyama, 950-8739 Niigata, Japan.
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Hsu D, Sandborg C, Hahn JS. Frontal lobe seizures and uveitis associated with acute human parvovirus B19 infection. J Child Neurol 2004; 19:304-6. [PMID: 15163099 DOI: 10.1177/088307380401900413] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/14/2022]
Abstract
We report a 5-year-old girl who developed repeated episodes of behavioral alterations shortly after human parvovirus B19 infection and uveitis. Video-electroencephalographic study demonstrated that these brief episodes were frontal lobe seizures. Seizures responded promptly to antiepilepsy medications. Further diagnostic testing did not reveal any rheumatologic disorders. Human parvovirus B19 infections in children are more commonly associated with febrile seizures and meningoencephalitis. Our case demonstrates that, rarely, it may be associated with the development of partial epilepsy.
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Affiliation(s)
- David Hsu
- Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Lucile Packard Children's Hospital at Stanford, California 94305-5235, USA
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Nolan RC, Chidlow G, French MA. Parvovirus B19 encephalitis presenting as immune restoration disease after highly active antiretroviral therapy for human immunodeficiency virus infection. Clin Infect Dis 2003; 36:1191-4. [PMID: 12715316 DOI: 10.1086/374603] [Citation(s) in RCA: 39] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/02/2002] [Accepted: 01/10/2003] [Indexed: 12/19/2022] Open
Abstract
Illness occurring during the initial months of highly active antiretroviral therapy (HAART) for human immunodeficiency virus infection may be a consequence of the restoration of an immune response against opportunistic pathogens (i.e., immune restoration disease [IRD]). We describe a young man who had AIDS complicated by parvovirus B19 infection and RBC aplasia and who developed a painless, progressive dyspraxia of the left arm and an expressive dysphasia 4 weeks after commencing effective HAART. Neuroimaging demonstrated multiple right fronto-parietal lesions, and, following extensive investigations, including a brain biopsy, it was concluded that the brain lesions represented IRD associated with parvovirus B19 infection.
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Affiliation(s)
- Richard C Nolan
- Department of Clinical Immunology and Biochemical Genetics, Royal Perth Hospital, Perth WA-6001, Australia.
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