Human parvovirus was first described in 1975(1). Human parvovirus B19 (B19V) is a human pathogenic virus, a member of erythrovirus genus in the parvoviridea family (2). B19 is a small, non-enveloped, ssDNA virus and, like all parvoviruses, the capsid proteins are arranged with icosahedral symmetry. B19 is 20-25 nm in diameter and has a genome of 5-6 kb (3). The B19 capsid is composed of two capsomer proteins, VP1 and VP2 which are encoded by overlapping reading frames (4). The structural proteins determine many of the biological properties of the virus, including binding to cell receptor, haemoagglutination and induction of neutralizing responses (5). A number of nonstructural proteins has been identified, the major nonstructural protein NS1(4). NS1 is an activating transcription factor for the single promoter of B19. In addition, NS1 nicks the replicative form of the viral genome at the origin of replication, allowing for replication of the viral DNA (6). The virus is transmitted through exposure to infected droplets or blood products and vertically from mother to fetus. Noscomial transmission has also been documented. The incubation period of the infection ranges from four to 14 days but can last as long as 21 days (7).
B19 infection is common infection. Its seroprevalence increases with age, from 2-10% of children under 5 years old, to 40-60% in adults more than 20 years old, and up to 85% in the elderly population. Infection is more common in the late winter and early summer, with epidemics peaks every 3-4 years (8).
The infection can occur asymptomatically or can be associated with a wide range of clinical features, such as erythema infectiosum, post infectious arthropathy and transient aplastic crises in patients with hemolytic anaemia. Chronic infections can also occur mainly in immunocompromised patients (9).
Generally, erythema infectiosum is self-limited and does not require treatment. Patients with arthralgia may require nonsteroidal anti-inflammatory drug treatment. Patients in transient aplastic crises may require erythrocyte transfusion while the marrow recovers. Chronic red cell aplasia, if severe may require intravenous immunoglobulin therapy. This treatment may improve anemia symptoms, but it may precipitate a rash or arthropathy. Intravenous immunoglobulin also has been in several case reports of severe illness (7). Although vaccine development has shown promising initial results, the is no currently vaccine available against parvovirus B19 (10).
Infection with parvovirus during pregnancy is not associated with increased risk of fetal malformation. However, infection during pregnancy is an important cause of intrauterine fetal death, stillbirth, and non-immune hydropsfetalis(11).
Maternal infection in pregnancy is a potential hazard to the fetus because of the virus ability to infect fetal erythroid precursor cells and fetal tissues (9). The fetus is particularly vulnerable to B19 infection because it has a rapidly expanding red-cell volume and relatively short red cell life span and because it may be unable to mount an effective immune response (12). The first association between parvovirus B19 infection in pregnancy and poor outcomes was reported in 1984, when hydropic fetuses were shown to have anti-B19 immunoglobulin M (IgM) (13). By increasing gestation age, the incidence of infection and fetal death decrease. If the mother has B19-specific antibodies, immunoglobulin G (IgG) against the virus, there will be no possibility of virus transition to the fetus (14).
The role of innate immunity in contrasting B19 virus infection has not been investigated in detail. Antibodies are the hallmark of the adaptive immune response to B19. In naïve individuals, B19 specific antibodies are produced early after infection and are assumed to be able to neutralize viral infectivity and progressively lead to clearance of infection. Immunoglobulin M (IgM) are produced first and can usually last about 3-6 months following infection, soon followed by production of immunoglobulin G (IgG) that is assumed to be long-lasting. Immunoglobulin A (IgA) can also be detected in body fluids (2).
If laboratory testing is needed, there are two types of diagnostic tests to confirm parvovirus infection: B19 specific antibody testing or viral DNA testing (7). In early studies, acute B19 infection was determined by demonstrating virus in serum by counter current immunoelectrophoresis (CIE) and immune electron microscope (IEM), tests that require serum specimens to be collected during the initial phase of infection when viral titer is high(15). In vitro the virus can be cultured in some erythromegakaryoblastoid cell lines, but replication is very inefficient (16).
Although B19 can be detected in serum by electron microscope (EM), B19 antigen enzyme linked immune sorbent assays (ELISA), and even hemoagglutination, B19 virus is usually detected by isolation of viral DNA by direct hybridization or Polymerase chain reaction (PCR)(17).The sensitivity of DNA hybridization tests can be increased by amplification of either target or the detector system. The most widely used method is amplification of the target by the polymerase chain reaction (18).The advent of PCR has greatly increased the sensitivity of DNA detection in serum and tissue samples, although it poses a great propensity of contamination (17).
There is no much published data concerning the determination of the prevalence of parvovirus B19 among Sudanese pregnant women using nested PCR, in a study conducted by Adam. et al in Sudan (2015), which was based on serology and B19 DNA was not detected in any of the samples (24), another study conducted by Maksheed M. et al in Kuwait (1999) (25), which was also based on detecting B19 antibodies only. In addition to a study conducted by Barros De Freitas in Brazil (1999) which detected B19 DNA in only one mother(26), and B19 antibodies were also detected in pregnant women under different gestation trimesters by Mirambo MM. et al in Tanzania ( 2017)(27).