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Since its discovery, human parvovirus B19 (B19V), now termed erythrovirus, has been associated with many clinical situations (neurological and myocardium infections, persistent B19V DNAemia) in addition to the prototype clinical manifestations, i.e., erythema infectiosum and erythroblastopenia crisis. In 2002, the use of new molecular tools led to the characterization of three different genotypes of human B19 erythrovirus. Although the genomic organization is conserved, the geographic distribution of the different genotypes varies worldwide, and the nucleotidic divergences can impact the molecular diagnosis of B19 virus infection. The cell cycle of the virus remains partially unresolved; however, recent studies have shed light on the mechanism of cell entry and the interactions of B19V proteins with apoptosis pathways.Before the recent descriptions of human bocavirus (2) and human parvovirus 4 (PARV4) (41), parvovirus B19 ([B19V] or erythrovirus B19) was the only known member of the Parvoviridae family to infect humans. The Erythrovirus genus contains B19V, erythroviruses that infect several simian species, and the parvovirus from Manchurian chipmunks (87a). These viruses share the remarkable property of replicating in and destroying erythroid progenitors. This strong in vitro tropism explains the difficulties in studying the replicative cycle of these viruses; indeed, the in vitro production and culture of erythroid progenitor cells remain delicate. An infectious B19V clone was described only recently (102), and its use, although mostly limited and allowing only a small amount of progeny production, led to constructions of recombinant viruses that were helpful in understanding the steps of the virus life cycle and the toxicity of the virus. Discovered in 1975 (19), B19V can cause a wide range of mild and self-limiting clinical manifestations, such as erythema infectiosum (fifth disease) and oligoarthritis (98). B19V infection can also cause acute anemia by aplastic crisis in patients whose red blood cells have shortened survival times (i.e., patients with sickle cell disease, thalassemia, spherocytosis, or any disorder of hemoglobin gene expression or red cell membrane constitution), chronic anemia in patients with congenital immunodeficiencies or human immunodeficiency virus (HIV) infection or who are undergoing chemotherapy for malignancies or organ transplants (48, 58), and hydrops fetalis or intrauterine death in infected fetuses (86). Recently, cases of neurological manifestations have been associated with B19V infection (22), as have myocardium infections (4,5,47,83), and the spectrum of B19V-linked diseases may further increase. CLINICAL MANIFESTATIONSThe primary route of transmission of B19V is the respiratory tract (via aerosol droplets), with a majority of infections occurring during childhood, but the infection may also be transmitted by organ transplantation and especially by transfusion of blood components, in particular by packed red cells from blood collected during the short preseroconversion vi...

Since the development of the first assay in 1989 (20), assays for detection of hepatitis C virus (HCV) antibodies (Ab) have allowed progress in the early detection of HCV infection (46). This increased sensitivity of the last-generation assays has dramatically reduced the risk of HCV transmission by blood components by reducing the window period from 82 days (5) to 66 days (3, 12). To further reduce the residual risk (2,5,16,18,36,37,41,48), nucleic acid testing (NAT) for HCV RNA was introduced in several high-income countries (2,14,15,21,30,39). In some countries, an assay for the detection of HCV core antigen (Ag) by use of the enzyme immunoassay (EIA) technology has been chosen as an alternative to NAT for the early diagnosis of infection (1,8,25,38). In addition, some authors emphasized the clinical advantage of HCV core Ag quantification as a direct marker of viral replication in the chronic phase of infection (4) and as a relevant marker for predicting and monitoring the response to therapy (7,29,31). Indeed, the HCV core Ag assays have sensitivities close to that of NAT, with mean detection differences of 1 to 2 days in the window period with the specific assay developed for blood screening (11,32,35,45) and 0.29 day with the immunoassay capable of detecting and quantifying HCV core Ag (23). A recent study reported that a prototype assay based on the simultaneous detection of HCV core Ag and anti-HCV Ab significantly closed the time gap between HCV RNA detection and the first appearance of detectable anti-HCV Ab (42). However, this assay is not yet available for routine use. More recently, a new combination assay has been developed and licensed in Europe (Monolisa HCV Ag/Ab ULTRA; Bio-Rad, Marnes la Coquette, France). To assess its sensitivity for the detection of HCV infection during the window period or at the early phase after seroconversion, we tested two panels and compared the results with those obtained using the two available assays for HCV Ag (HCV core Ag EIA blood screening assay and trak-C assay) and HCV RNA. The overall objective was to determine if this new test could constitute an alternative to NAT for the diagnosis of HCV infection during the window period and whether the sensitivity for antibody detection is preserved. (Table 1) consisted of 12 blood donor samples which were negative for anti-HCV Ab (Ortho HCV 3.0 EIA test system Enhanced SAVe; Ortho Clinical Diagnostics, Raritan, NJ) but positive for HCV RNA. The plasma from each of these blood donations was immediately aliquoted and stored at Ϫ30°C until it was MATERIALS AND METHODS Panels

Human parvovirus 4 infections are primarily associated with parenteral exposure in western countries. By ELISA, we demonstrate frequent seropositivity for antibody to parvovirus 4 viral protein 2 among adult populations throughout sub-Saharan Africa (Burkina Faso, 37%; Cameroon, 25%; Democratic Republic of the Congo, 35%; South Africa, 20%), which implies existence of alternative transmission routes.

This new developed assay presents an improvement for the detection of HCV infection, especially in the early phase of infection when antibodies are undetectable. Although less sensitive than NAT, this assay could be a suitable solution for blood screening in developing countries where NAT (or HCV core antigen-specific assay) is not affordable or its implementation is not feasible.

Immunity to human group A rotavirus (RV), a major cause of viral gastroenteritis in infants, involves B lymphocytes that provide RV-specific antibodies. Additionally, some arguments suggest that naive B cells could be implicated in the first steps of the immune response against RV. The aim of our study was to analyze the interaction of VP6 and VP7 RV capsid proteins with human B cells depending on the immune status of the individual, i.e., naive or RV experienced. For this purpose, a two-color virus-like particle flow cytometry assay was devised to evaluate the blood B-lymphocyte reactivity to VP6 and VP7 proteins from healthy RV-exposed adults, recently infected infants, and neonates at birth. Both VP6 and VP7 interactions with B cells were mediated by surface immunoglobulins and probably by their Fab portions. VP7-reactive B lymphocytes were mainly detected from RV-experienced patients and almost exclusively in the CD27-positive memory cell fraction. Conversely, VP6-reactive B lymphocytes were detected at similar and high frequencies in adult, infant, and neonate samples. In adult samples, VP6 reacted with about 2% of the CD27-negative (CD27 neg ) naive B cells. These results demonstrated that the VP6 RV protein interacted with a large fraction of naive B lymphocytes from both adults and neonates. We propose that naive B cell-VP6 interaction might influence the strength and quality of the acquired immune response and should be considered for elaborating RV vaccine strategies.Human group A rotavirus (RV) is recognized as a leading cause of severe dehydrating diarrhea in young children. The worldwide impact of the disease has led to extensive research to develop RV vaccines (15,16,29). However, RV vaccines only partially achieve protective immunity in humans, as do natural primary exposures. The previously released Rotashield vaccine, which has been withdrawn because of adverse effects, conferred only a 60% level of protection against RV-induced diarrhea (1, 35). The bases underlying the variable efficacy of RV vaccines are unknown. Efforts remain to be made to better understand the protective mechanisms against RV for improving vaccine strategies.RV possesses a triple-layered icosahedral protein capsid, and three of the RV structural proteins (VP4, VP6, and VP7) have important antigenic properties. The intermediate-layer capsid protein VP6 mediates group and subgroup specificity, while the outer-layer proteins VP4 and VP7 mediate serotype P and serotype G specificities, respectively (20). VP6 is the most immunogenic RV protein (20, 34). VP6 does not induce neutralizing antibodies (Abs), although some VP6-specific polymeric immunoglobulins A (IgA) are protective in vivo, probably via transcytosis through epithelial cells (6, 32). VP7 is known as the major antigen inducing neutralizing Abs (20). These Abs can passively protect experimental animals from RV-induced diarrhea (26,30,31). In humans, RV-induced Abs probably play an important role in the resolution of viral infection and against reinfections, as suggest...

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