Free Essay On Human Bocavirus Is Not A Clinically Significant Human Pathogen

Type of paper: Essay

Topic: Viruses, Medicine, Vaccination, Disease, Human, Aliens, Infection, Health

Pages: 4

Words: 1100

Published: 2021/02/03

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Introduction

The human Bocavirus (HBoV) is a novelty in the medical field as it was just a recently discovered pathogen in 2005. Liu (2011) indicated that its origin is from the Parvoviridae family of virus. There are growing debates about the HBoV epidemiologic contribution as independent causative agent in other diseases, such as respiratory disease and gastroenteritis based on its clinical presentation, with the presence of co-infections that add to the complexities of clinical findings, which this paper seeks to obtain better clinical insights based on the various literatures and clinical studies about the human Bocavirus.

Discussion

The human Bocavirus is highly associated with respiratory tract infection and gastrointestinal diseases, but clinical researches fail to fully establish its role as an independent causative factor. Four genotypes of HBoV (HBoV1-4) have been described namely the HBoV-1 that is associated with respiratory tract infections and HBoV-2, -3, and -4 genotypes that are considered as entero-pathogenic. Their exact role largely remains unclear. Conflicting studies are present that show that the virus is a mere harmless bystander instead of a true pathogen (Schildgen, 2013) due to the presence of co-infections. Debates involving the clinical studies about HBoV devolve to the non-conformity on Koch’s principle of temporality where to be a causative agent, the virus must be solely responsible for the infection preceding the disease manifestation (Pellet, 2015). Schildgen, et al. (2008) also postulates that the non-conformity exists owing to the genetic difference of HBoV1 from other human respiratory viruses and it co-exists with them, while Moriyama (2010) signifies that it sheds from asymptomatic individuals for years. The same amount of viral load in both asymptomatic and symptomatic patients is also perplexing considering that the prolonged presence of the virus results in multiple exposures to allelic variants that evoke immunity and shedding is viewed as a potential mode of transmission (Martin et al, 2010). Christensen, et al. (2008) pointed out that among HBoV infected children, about 78% of them have multiple viral infections. This finding is consistent with the clinical studies conducted by Wang, et.al (2010), showing that the HBoV infection always occurs with other viruses in respiratory tract infections among children. Zheng et al. (2010) state that neither co-infection nor the severity of disease correlated with the viral load, thus further studies need to prove the role of HBoV as a causative agent in the severity of the disease when it co-infects with other viruses such as influenza A viruses (Goka et al., 2014). 
The laboratory findings of increased neutrophils in the blood cell show some pathogenic potential of HBoV in young children with the LRTI (Moriyama, 2010). Arnold, Singh, Spector and Sawyer (2015) that further studies are needed in order to establish HBoV as the causative agent in LRTI. Deng, et. al. (2012) supports the same finding, hypothesizing that the HBoV can have a significant role in causing the LRTI among children as an etiologic agent that cause wheezing and long term hospitalization. Supporting this hypothesis, the researchers point out that the HBoV is present even among children with asymptomatic respiratory tract secretions. The clinical study of Allander, et.al (2007) support the finding that the human Bocavirus with high viral loads is associated with respiratory tract infections, while those with low viral load indicates viral shedding. Manning, et.al (2006) also provides in their research that there is a high predominance of the HBoV infections among children with co-infection. This hypothesis has been challenged by Venermo, et.al (2009) providing that there is no concrete indication to associate HBoV as a causative agent due to lack of study showing whether the co-infection of HBoV with other viruses is a sequential infection or a simultaneous viral infection.
In the presence of diarheal pathogens like the Rotavirus, B. Salmonella, Campylobacter and Staphylococcus Aureus, Lau (2007) explains that it is difficult to establish HBoV as the main causative factor in gastroenteritis. The virus was also detected in the respiratory secretions, serum and stools in stem cell transplant recipients, although it remains unclear how the virus disseminated the infection (Kahn, 2008). This is another area of potential research that human Bocavirus can cause viremia, which is the presence of virus in the blood (Diallo, 2005) during an infection. About 90.9% of patients in the study showed to be IgM positive, which is highest among children with a lower respiratory tract infection and pneumonia. Thus, it can be pointed out that the virus-specific IgM antibodies can be an additional marker to the acute infections manifested among the HBOv positive patients (Karalar, 2010). There is a very low frequency for the HBoV to be present in the COPD acute exacerbations, making it unlikely to consider HBoV as a trigger (Ringshausens, et. al. 2009). In Kawasaki disease, the area of consideration is on the genetic susceptibility of children as a result of hyper immune reaction. However, the presence of suspected viral agents like the Adenovirus, Parvovirus, Parainfluenza virus, HIV, measles, Varicella-zoster virus and Rotavirus were not isolated (Santos, et. al. 2010). Studies on the presence of HBoV DNA in lung (18%) and colorectal cancer (20%) cells suggest that HBoV might have an implicative role in the development of these forms of cancers (Schildgen, 2013). A possible association of HBoV 1-2 with encephalitis has also been reported, where the cerebrospinal fluid contained HBoV like nucleotide sequence and particles exclusively (Mitui et al. 2012).

Conclusion

In conclusion, although the presence of HBoV in respiratory diseases and gastroenteritis has been identified, its role as a causative agent remains questionable and doubtful. This observation is however not conclusive to state that the human Bocavirus has not established itself as a potential pathogenic agent in respiratory diseases (Farrar, 2009), however, the high presence of co-infections with other respiratory viruses may complicate the analysis of the clinical studies made on the human Bocavirus (Guido, 2011). To clinically establish the role of the HBoV as a causative agent, other viruses must be isolated. Until then, it can be concluded that the virus is not a clinically significant human pathogen.

References:

Allander, et.al (2006). Human bocavirus and acute wheezing in children. Clinical Infectious Disease. 44:904-910.
Arnold, J.C., Singh, K.K., Spector, S.A. and Sawyer, M.H. 2015. Human bocavirus:Prevalence and clinical spectrum at a Children’s Hospital. Clinical infectious disease. 43:283-288.
Christensen, A. et al. 2008. Human bocavirus commonly involved in multiple viral airway infections. Journal of clinical virology. 41: 34-37.
Deng, Y. et. al. 2012. High viral load of boavirus correlates with duration of wheezing in children with severe lower respiratory tract infection. PlosOne. 7(3):1-7.
Diallo, A. 2005. Microbiology Recall. Maryland: Lippincott Williams and Wilkins.
Farrar, J. 2009. Manson;s Tropical Diseases. 23rd Ed. China: Elsevier.
Guido, M. 2011. Seroepidemiology of human bocavirus in Apulia, Italy. Clinical Microbial Infection. 18:74-76.
Kahn, J. 2008. Human bocavirus: Clinical significance and implications. Current opinion in pediatrics. 20:62-66.
Karalar, L. 2010. Prevalence and clinical aspects of human bocavirus infection in children. Clinical Microbial Infection. 16: 633-639.
Lau, S.K. 2007. Clinical and molecular epidemiology of human bocavirus in respiratory and fecal samples from children in Hong Kong. The Journal of Infectious Disease. 196: 986-993.
Liu, D. 2011. Molecular detection of human viral pathogens. Florida: CRC Press.
Manning, A. et.al. 2006. The Journal of infectious disease. 194: 1283-1290.
Moriyama, Y. 2010. Distinctive clinical features of human bocavirus in children younger than 2 years old. European Journal Pediatrics. 169: 1087-1092.
Ringshausen, F.C. et. al. 2009. Frequency and clinical relevance of human bocavirus infection in acute exacerbation of COPD. International Journal of COPD. 4: 11-117.
Santos, R. et. al. 2010. Kawasaki Disease and the Human Bocavirus – Potential Association. Journal of Microbiology Immunology and Infection.
Schildgen, O. 2013. Human Bocavirus: Lesson learned today. Pathogens. 2:1-12.
Schildgen, O. et.al. 2008. Human Bocavirus: Passenger or pathogen in acute respiratory tract infections? Clinical Microbiology Review. 21(2): 291-304.
Venermo, M. et.al. 2009. Clinical assessment and improved diagnosis of Bocavirus induced wheezing in children, Finland. Emerging infectious disease. 15(9): 1423-1430.

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