The Mechanism of Infection of the Hantavirus - Essay Example

The N protein introduces the virus into the cytoplasm of the healthy human cell (Mir, 2010). The N protein of the virus associates itself with the L protein of the human host and produces “capped primers” or nucleocapsids, which can initiate transcription of the viral mRNAs upon invasion of the healthy human cell.

Meanwhile, the glycoproteins G1 and G2 are transported to the Golgi bodies from the ER. Once the nucleocapsids interact with the glycoproteins, hantavirus is formed and is released out of the cell through exocytosis (“Virology,” CDC, 2011). Once the virions are out of the plasma membrane, the symptoms of HFRS or HPS begin showing. The replication of the hantavirus occurs in the macrophages and vascular endothelial cells of the human lungs and kidneys (Muranyi et al., 2005). However, symptoms do not show until the replication process of a particular number of virions is finished and until these virions are released out of the plasma membrane to infect other cells.

The endothelial cells of the lungs and kidneys are the main target cells of the virus. The endothelial cells are responsible for various physiologic functions of the body such as the regulation of edema, vascular repair, and gas exchange (Mackow & Gavrilovskaya, 2009). Therefore, it simply follows that someone who is infected with the hantavirus will have problems with these physiologic functions. The young man in the case study exhibited shortness of breath and labored and rapid breathing because the hantavirus has already invaded the endothelial cells of his lungs, which are responsible for gas exchange.

Thus, the physiological ability of his lungs to handle gas exchange is impaired. According to Mir (2010), the hantavirus also infects mature and immature dendritic cells. Dendritic cells are responsible for capturing antigens and inducing a primary immune response among T lymphocytes (Wieder, 2003). However, the hantavirus uses the dendritic cells as vehicles of transport through the lymphatic system where the virus can infect monocytes and macrophages (Mir, 2010). Moreover, the ultimate result of the destruction of the endothelial cells and the white blood cells by the hantavirus is “damage to capillaries and small vessel walls,” which eventually lead to “vasodilation and congestion with hemorrhages” (“Hantavirus,” Kenyon.edu, 2011).

These are the symptoms of the disease and the most probable cause of death in the young man in the case study before he died. Furthermore, the cause of his immediate death may have also been the fact that the hantavirus has already destroyed most of the monocytes and macrophages in his body. The destruction of these white blood cells meant that the virus was allowed to freely replicate in and infect the young man’s lung cells. Another possible reason why the hantavirus was so virulent that it caused the death of a young man in only a matter of days was the five-nanometer lipid bilayer that surrounds the virus (“Hantavirus Infections,” 2006).

This lipid bilayer envelope contains the antigens of the glycoprotein needed to infect the healthy human cell (Manigold et al., 2010). Therefore, without the bilayer, the hantavirus will lose its virulent properties since there would be nothing to house the antigens. Moreover, this lipid bilayer contains three nucleocapsids (“Hantavirus,” Kenyon.edu, 2011). These nucleocapsids interact with the glycoproteins inside the human cell and form the hantavirion. The hantavirion is then transported out of the cell for further infection.