Background
In 2005, Swedish scientists discovered a new virus similar to the known parvovirus during a large-scale screening of samples of acute upper respiratory tract infections in children. Because of its high homology with bovine and canine bocaviruses, it was named human bocavirus (HBoV). Later, researchers found HBoV2 in the feces of children with acute flaccid paralysis without polio infection, and HBoV3 and HBoV4 were also discovered. In terms of taxonomy, HBoV is considered to belong to the genus Bocavirus of the subfamily Parvovirinae of the family Parvoviridae. HBoV is the second type of parvovirus discovered to date that can infect humans after parvovirus B19. According to the results of whole genome sequencing and sequence analysis of HBoV, HBoV can be divided into four types: HBoV1, HBoV2, HBoV3 and HBoV4. It has not yet been determined whether the four types of HBoV represent different virus strains or different genotypes of the same virus strain. Existing research results show that HBoV is not only a pathogen of respiratory diseases, but may also be a pathogen that causes acute gastroenteritis in children.
Figure 1. Electron microscopic analysis of human bocavirus (HBoV) viral protein 2 (VP2) viruslike particles (VLPs). (Sources: Lindner J, et al. 2008)
The HBoV genome is a single-stranded linear DNA with a total length of about 5.6 kb. Its morphology is very similar to other parvoviruses. It is a type of non-enveloped small particle virus with a particle diameter of 20 to 25 nm under an electron microscope. The genome structure of type 4 HBoV is basically the same. There are three open reading frames from 5' to 3', two of which encode non-structural proteins NS1 and NP1, respectively, and the other encodes two viral capsid proteins VP1 and VP2. VP1 and VP2 have typical gene overlap regions. In addition, VP1 also has a non-overlapping region, namely the VP1 unique region (VP1u). The 5' left-end hairpin (LEH) and the 3' right-end hairpin (REH) have a serpentine sequence, forming a stem-loop and hairpin-like complex secondary structure. The NS1 gene of parvovirus was transcribed and translated first, and it has been confirmed that it plays a super-activation role in the process of viral replication; the non-structural protein NP1 is related to viral replication and plays an important role in escaping the host's inherent immunity. HBoV VP1 has phospholipase A2-like activity, which plays an important role in viral infection of the human body and can help the virus enter the cell nucleus from the cytoplasm for gene replication and transcription. The VP1 and VP2 genes are relatively conservative, and the VP1 and VP2 proteins have good antigenicity, so they are often used in HBoV serological detection. Some studies have expressed HBoV1 VP1u and VP2 proteins in prokaryotes, and used immunospot technology to detect HBoV1 IgG and IgM in the serum of children with asthma. The results showed that compared with VP1u, VP2 has stronger immune activity, proving that VP2 is an ideal antigen for HBoV serological detection. Therefore, more studies are currently targeting the production of monoclonal antibodies against VP2 structural proteins and establishing rapid virus detection methods, which can be conveniently used in clinical work.
HBoV DNA has been detected in different types of specimens, among which HBoV1 and HBoV2 DNA have the highest detection rates. The detection rate of HBoV1 DNA in respiratory specimens is relatively high, and HBoV2 DNA is mainly detected in digestive specimens. There is still no unified standard for the diagnosis of HBoV infection. Because the in vitro culture system and animal model for HBoV are not yet mature, PCR amplification of HBoV genomes in clinical samples is mainly used for detection. The establishment of ELISA, immunoblotting, and immunofluorescence detection can be further used for the detection of HBoV IgG and IgM antibodies in serum. Electron microscopy technology can also be used for virus detection. However, because the preparation of electron microscopy specimens is relatively cumbersome and expensive, it is limited in the detection of HBoV infection and is currently mainly used for the observation of the morphological structure of the virus.
Alternative Names
HBoV
Bocavirus
Human Bocavirus 1
Parvovirus
Human Parvovirus Bocavirus
References
- 1. Lindner J, et al. CD4+ T helper cell responses against human bocavirus viral protein 2 viruslike particles in healthy adults. J Infect Dis. 2008, 198(11):1677-84.
References
Human Bocavirus in Childhood: A True Respiratory Pathogen or a "Passenger" Virus? A Comprehensive Review
Microorganisms
Authors: Trapani S, Caporizzi A, Ricci S, Indolfi G
Abstract
Recently, human bocavirus (HBoV) has appeared as an emerging pathogen, with an increasing number of cases reported worldwide. HBoV is mainly associated with upper and lower respiratory tract infections in adults and children. However, its role as a respiratory pathogen is still not fully understood. It has been reported both as a co-infectious agent (predominantly with respiratory syncytial virus, rhinovirus, parainfluenza viruses, and adenovirus), and as an isolated viral pathogen during respiratory tract infections. It has also been found in asymptomatic subjects. The authors review the available literature on the epidemiology of HBoV, the underlying risk factors associated with infection, the virus's transmission, and its pathogenicity as a single pathogen and in co-infections, as well as the current hypothesis about the host's immune response. An update on different HBoV detection methods is provided, including the use of quantitative single or multiplex molecular methods (screening panels) on nasopharyngeal swabs or respiratory secretions, tissue biopsies, serum tests, and metagenomic next-generations sequencing in serum and respiratory secretions. The clinical features of infection, mainly regarding the respiratory tract but also, though rarely, the gastrointestinal one, are extensively described. Furthermore, a specific focus is dedicated to severe HBoV infections requiring hospitalization, oxygen therapy, and/or intensive care in the pediatric age; rare fatal cases have also been reported. Data on tissue viral persistence, reactivation, and reinfection are evaluated. A comparison of the clinical characteristics of single infection and viral or bacterial co-infections with high or low HBoV rates is carried out to establish the real burden of HBoV disease in the pediatric population.
Human bocavirus respiratory infection: Tracing the path from viral replication and virus-cell interactions to diagnostic methods
Rev Med Virol
Authors: Colazo Salbetti MB, Boggio GA, Moreno L, Adamo MP
Abstract
Human bocaviruses were first described between 2005 and 2010, identified in respiratory and enteric tract samples of children. Screening studies have shown worldwide distribution. Based on phylogenetic analysis, they were classified into four genotypes (HBoV1-4). From a clinical perspective, human bocavirus 1 (HBoV1) is considered the most relevant, since it can cause upper and lower acute respiratory tract infection, mainly in infants, including common cold, bronchiolitis, and pneumonia, as well as wheezing in susceptible patients. However, the specific processes leading to structural, biochemical, and functional changes resulting in the different clinical presentations have not been elucidated yet. This review surveys the interactions between the virus and target cells that can potentially explain disease-causing mechanisms. It also summarises the clinical phenotype of cases, stressing the role of HBoV1 as an aetiological agent of lower acute respiratory infection in infants, together with laboratory tests for detection and diagnosis. By exploring the current knowledge on the epidemiology of HBoV1, insights into the complex scenario of paediatric respiratory infections are presented, as well as the potential effects that changes in the circulation can have on the dynamics of respiratory agents, spotlighting the benefits of comprehensively increase insights into incidence, interrelationships with co-circulating agents and potential control of HBoV1.
COA
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