Research progress on the infection of hemorrhagic fever viruses to respiratory tract

doi:10.3877/cma.j.issn.1674-1358.2023.01.003

Abstract

Abstract:

Viral hemorrhagic fevers (VHFs) is a group of acute infectious diseases caused by a variety of viruses with fever, shock and hemorrhage as the main clinical symptoms. VHFs are globally spreaded and with a high mortality, posing a serious risk to human health. In recent years, VHFs such as dengue fever, hemorrhagic fever with renal syndrome and Ebola virus disease had continued to be prevalent, posing a serious challenge to global public health security. The pathogenesis of VHFs are still not well studied and there is no specific treatment for most of these diseases. The respiratory tract is not only an important way for the human body to be exposed to hemorrhagic fever virus, but also an important site for the body to produce immune response, and an important organ for damage in various VHFs. It is of great significance to study the infection of respiratory tract and reveal the mechanism of respiratory tract lesions caused by hemorrhagic fever virus, which is of great significance to investigate the pathogenesis of VHFs infection and its severe process, and to research the prevention and treatment measures. This paper reviews the biological status of the infection of respiratory tract caused by common hemorrhagic fever viruses such as dengue virus, hantavirus and Ebola virus.

Key words: Viral hemorrhagic fever, Respiratory tract, Viral infection

Kaixuan Zhang, Yan Liang, Hongyan Shi, Xuyang Zheng, Jianqi Lian, Qianqian Zhang. Research progress on the infection of hemorrhagic fever viruses to respiratory tract[J]. Chinese Journal of Experimental and Clinical Infectious Diseases(Electronic Edition), 2023, 17(01): 12-15.

/ / Recommend

Add to citation manager EndNote|Ris|BibTeX

URL: https://zhsyhlcgrbzz.cma-cmc.com.cn/EN/10.3877/cma.j.issn.1674-1358.2023.01.003

https://zhsyhlcgrbzz.cma-cmc.com.cn/EN/Y2023/V17/I01/12

References 27

[1]	Yu X, Cheng G. Contribution of phylogenetics to understanding the evolution and epidemiology of dengue virus[J]. Animal Model Exp Med,2022,5(5):410-417.
[2]	Crowcroft NS, Infuso A, Ilef D, et al. Risk factors for human hantavirus infection: Franco-Belgian collaborative case-control study during 1995-6 epidemic[J]. BMJ,1999,318(7200):1737-1738.
[3]	Lee YR, Su CY, Chow NH, et al. Dengue viruses can infect human primary lung epithelia as well as lung carcinoma cells, and can also induce the secretion of IL-6 and RANTES[J]. Virus Res,2007,126(1-2):216-225.
[4]	Wei X, Meng B, Peng H, et al. Hemorrhagic fever with renal syndrome caused by destruction of residential area of rodent in a construction site: epidemiological investigation[J]. BMC Infect Dis,2022,22(1):761.
[5]	杨晓燕, 聂俊峰, 赵莹, 等. 2015-2019年广州市番禺区598例登革热患者感染特征[J]. 热带医学杂志,2021,21(12):1597-1600.
[6]	Qiu M, Zhao L, Zhang J, et al. Effective infection with dengue virus in experimental neonate and adult mice through the intranasal route[J]. Viruses,2022,14(7):1394.
[7]	Rojek A, Horby P, Dunning J. Insights from clinical research completed during the west Africa Ebola virus disease epidemic[J]. Lancet Infect Dis,2017,17(9):e280-e92.
[8]	Uyeki TM, Mehta AK, Davey RT,et al. Clinical management of Ebola virus disease in the United States and Europe[J]. N Engl J Med,2016,374(7):636-646.
[9]	Johnson E, Jaax N, White J, et al. Lethal experimental infections of rhesus monkeys by aerosolized Ebola virus[J]. Int J Exp Pathol,1995,76(4):227-236.
[10]	Reed DS, Lackemeyer MG, Garza NL, et al. Aerosol exposure to Zaire ebolavirus in three nonhuman primate species: differences in disease course and clinical pathology[J]. Microbes Infect,2011,13(11):930-936.
[11]	Weingartl HM, Embury-Hyatt C, Nfon C, et al. Transmission of Ebola virus from pigs to non-human primates[J]. Sci Rep,2012,2(1):811.
[12]	Nfon CK, Leung A, Smith G, et al. Immunopathogenesis of severe acute respiratory disease in Zaire ebolavirus-infected pigs[J]. PLoS One,2013,8(4):e61904.
[13]	Rasmuson J, Lindqvist P, Sörensen K, et al. Cardiopulmonary involvement in Puumala hantavirus infection[J]. BMC Infect Dis,2013,13:501.
[14]	Rasmuson J, Pourazar J, Linderholm M, et al. Presence of activated airway T lymphocytes in human puumala hantavirus disease[J]. Chest,2011,140(3):715-722.
[15]	Hägele S, Nusshag C, Müller A, et al. Cells of the human respiratory tract support the replication of pathogenic Old World orthohantavirus Puumala[J]. Virol J,2021,18(1):169.
[16]	Bourquain D, Bodenstein C, Schürer S, et al. Puumala and Tula virus differ in replication kinetics and innate immune stimulation in human endothelial cells and macrophages[J]. Viruses,2019,11(9):855.
[17]	Mayor J, Torriani G, Rothenberger S, et al. T-cell immunoglobulin and mucin (TIM) contributes to the infection of human airway epithelial cells by pseudotype viruses containing Hantaan virus glycoproteins[J]. Virology,2020,543(4):54-62.
[18]	Torriani G, Mayor J, Zimmer G, et al. Macropinocytosis contributes to hantavirus entry into human airway epithelial cells[J]. Virology,2019,531(6):57-68.
[19]	Solà-Riera C, García M, Ljunggren HG, et al. Hantavirus inhibits apoptosis by preventing mitochondrial membrane potential loss through up-regulation of the pro-survival factor BCL-2[J]. PLoS Pathog,2020,16(2):e1008297.
[20]	Martínez VP, Di Paola N, Alonso DO, et al. "Super-spreaders" and person-to-person transmission of Andes virus in Argentina[J]. N Engl J Med,2020,383(23):2230-2241.
[21]	Sundström KB, Nguyen Hoang AT, Gupta S, et al. Andes Hantavirus-infection of a 3D human lung tissue model reveals a late peak in Progeny virus production followed by increased levels of proinflammatory cytokines and VEGF-A[J]. PLoS One,2016,11(2):e0149354.
[22]	Rowe RK, Pekosz A. Bidirectional virus secretion and nonciliated cell tropism following Andes virus infection of primary airway epithelial cell cultures[J]. J Virol,2006,80(3):1087-1097.
[23]	Deng B, Zhou B, Zhang S, et al. Clinical features and factors associated with severity and fatality among patients with severe fever with thrombocytopenia syndrome Bunyavirus infection in Northeast China[J]. PLoS One,2013,8(11):e80802.
[24]	Min YQ, Ning YJ, Wang H, et al. A RIG-1-like receptor directs antiviral responses to a bunyavirus and is antagonized by virus-induced blockade of TRIM25-mediated ubiquitination[J]. J Biol Chem,2020,295(28):9691-711.
[25]	Katti R, Shahapur PR, Udapudi KL. Impact of Chikungunya virus infection on oral health status: an observational study[J]. Indian J Dent Res,2011,22(4):613.
[26]	De Caluwé L, Heyndrickx L, Coppens S, et al. Chikungunya virus’ high genomic plasticity enables rapid adaptation to restrictive A549 cells[J]. Viruses,2022,14(2):282.
[27]	Wikan N, Sakoonwatanyoo P, Ubol S, et al. Chikungunya virus infection of cell lines: analysis of the East, Central and South African lineage[J]. PLoS One,2012,7(1):e31102.

Please choose a citation manager

Content to export