Hanta Virus

1. Introduction
Hantaviruses are the rodent borne viruses that cause severe clinical illness in human. Each strain of hantavirus is specific to a particular rodent host and cause and different clinical disease [1]. It belongs to the family of Bunyaviridae. The virus was recognized as a pathogenic virus in the previous decades. First case of hantavirus was diagnosed in 1993, during an endemic in Southwestern U.S. In human, it usually cause two types of disease including Hantavirus pulmonary syndrome (HPS) and Hantavirus hemorrhagic fever with renal syndrome (HFRS) [2]. Nephropathia epidemica (NE) is another disease caused by hantavirus, mostly seen in Europe.

2. Structure of Hantavirus
Hantaviruses are the enveloped viruses having three negative sense single-stranded RNA segments designated as small (S), medium (M) and large (L) as shown in Figure 1. S segment is involved in the coding of Nucleocapsid protein (NP) while M and L segments are coding for the surface envelope glycoproteins G1 & G2, and the RNA dependent RNA polymerase, respectively [3]. Its size ranges from 80 – 120 nm in dimeter. Minor open reading frames are also present in the viral genome but no corresponding protein has been reported till now. Nucleocapsid protein is the main structural protein of hantavirus, which is complexed with the viral RNA and forms the nucleocapsids [4].

3. Host of Hantavirus
The main host of hantavirus is the murid rodent. Previously it was thought that one rodent specie is a specific host for one strain of hantavirus, but later it became clear that multiple rodents can be hosts for one single strain of hantavirus [5]. Hantavirus infection was diagnosed in many animals e.g. dog,   cat, cattle, etc. But still there is no evidence that they are the host of hantavirus. Furthermore, humans also get the hantavirus infection but they are not the natural host of hantavirus. They get the infection accidentally through virus containing aerosolized rodent excretion such as urine, feces or saliva.

4. Replication cycle of Hantavirus
Virus attaches itself to the αVβ3 integrin on the cellular surface and enters the body through cellular membrane and this process is aided by the glycoproteins of the virus [6]. After entering the host cell, uncoating of virion occurs there. Then the nucleocapsids are released to the cytoplasm. Then transcription, translation and replication occur for the assembly of virus as shown in Figure 2. After that, virus is released by exocytosis.

5. Clinical features of disease caused by Hantavirus
Clinical symptoms of HPS, HFRS and NE resemble with each other, but there are some unique features observed in the infected patients.
5.1. Hantavirus Hemorrhagic Fever with Renal Syndrome (HFRS)
Symptoms of HFRS include high fever, backache, chills, abdominal pain, myalgia, malaise, etc. The disease caused various circulatory disorders hemorrhagic manifestations [7]. Only 15% of patients have severe form of disease while the fatality rate of disease is 15%.
5.2. Hantavirus Pulmonary Syndrome (HPS)
Symptoms of HPS include flu, headache and high fever. Patients with increased lactate level are more susceptible to get the severe form of disease. The approximate mortality rate of HPS is 50% [8].
5.3. Nephropathia epidemica (NE)
NE is the milder variant of HFRS having symptoms of high fever, headache, backache, and abdominal pain. Only 1% infected patients experience the severe form of disease, while others recover at an early stage [3].

6. Conclusion
Hantavirus is the alarming virus that can cause a pandemic if not controlled at the right time. At present there is no treatment available against hantavirus infections, so the only way to control the infection is the prevention. On the one hand, the only prevention forms this disease is to avoid the places where murid rodents live in large numbers. While, keep your surrounding clean can also help to be prevent from hantavirus. Furthermore, immediate treatment should be followed in case of hantavirus infection.

7. References
[1] J. Lee, “A Review on Orthohantavirus (Hantavirus),” IDOSR J. Exp. Sci., vol. 6, p. 7, 2020.

[2] P. PRADHAN and J. P. SAHOO, “85. A Short Note on Hantavirus,” IDOSR J. Exp. Sci., 2020.

[3] W. Muranyi, U. Bahr, M. Zeier, and F. J. Van Der Woude, “Hantavirus infection,” Journal of the American Society of Nephrology. 2005, doi: 10.1681/ASN.2005050561.

[4] A. Plyusnin, O. Vapalahti, and A. Vaheri, “Hantaviruses: Genome structure, expression and evolution,” Journal of General Virology. 1996, doi: 10.1099/0022-1317-77-11-2677.

[5] J. J. Scharninghausen, M. Faulde, and S. Cavaljuga, “Hantavirus host/virus interactions within Southeast Europe,” Bosn. J. Basic Med. Sci., vol. 4, no. 4, p. 13, 2004.

[6] K. R. Padma, K. R. Don, P. Josthna, and V. Bindu, “Globally Emerging Hantavirus Clinical Syndromes and Mechanism to Eradicate the Threat to Human Society-A Short Review.”

[7] B. Z. Sirotin and N. P. Keiser, “On the history of the study of haemorrhagic fever with renal
syndrome in eastern Russia,” Nephrol. Dial. Transplant., vol. 16, no. 6, pp. 1288–1289, 2001.

[8] A. Mahmud-Al-Rafat, M. E. Sobhani, and A. Taylor-Robinson, “Effects of anthropogenic events
and viral persistence on rodent reservoirs of hantavirus infection understanding host-pathogen
interactions facilitates novel approaches to intervention strategies,” 2015.

By: Rimsha Zafar