The Danger Behind the Mosquito Bite, Research Paper Example

The West Nile Virus is the virus behind several debilitating human diseases. Since its discovery in 1937, the life cycle of the virus has been studied closely in order to ascertain the routes by which the disease spreads through vectors and around the globe. Due to the fact that the virus has shown an acute ability to mutate, spreading from birds, to mosquito’s and finally to humans, scientists have given the disease a careful amount of diligent study in order to understand the virology of the West Nile virus (WNV).  Current scientific endeavors are underway, working to create a preventative vaccine for the West Nile virus in order to prevent this deadly pathogen from becoming more of a menace than it already is.

Since the 1990’s the West Nile Virus has become a significant threat to public health. Before the 1990’s, little was known of this somewhat rare disease. Since it was first isolated by scientists in 1937, the incidence of West Nile virus was relegated to the Eastern hemisphere, including Africa, Asia, the Middle East and Europe. Reports of human outbreaks were infrequent and only a mild febrile illness was associated with the disease (Center for Disease Control, 2007). After the 1990’s, however, the virus suddenly became more widespread. West Nile virus causes neuroinvasive disease in humans that is becoming more geographically widespread and invasive, causing scientists and centers for disease control  and research to spend more time studying the disease in order to understand its symptoms, modes of transmission and genetic nature so that preventative actions such as vaccines can be created in order to decrease the infection and mortality rate of the West Nile virus in human populations.

The symptoms and effects of the West Nile Virus range from non-existent to extreme. While 80% of those infected with the West Nile virus show no signs and no symptoms of being infected with the disease, about 20% will develop a mild infection known as West Nile fever. The signs and symptoms of West Nile fever can include nausea, vomiting, diarrhea, headache, backache, muscle aches, skin rash, swollen lymph nodes and a loss of appetite. Symptoms generally last between three to six days after which recovery is spontaneous and  complete (Sfakianos, and Hecht, 2009). West Nile virus in its more vicious and sometimes fatal form affects less than 1% of the population. In these cases, the disease causes either West Nile encephalitis, a swelling of the brain, or West Nile meningoencephalitis, which is the inflammation of the brain and the connective tissue membranes that surround and protect it. In rare cases, the disease manifests as West Nile poliomyelitis which attacks the spinal chord, causing it to become inflamed and weakened. In this case the affected person will suffer form a sudden and crippling weakness of the arms, legs and breathing muscles (Sfakianos, and Hecht, 2009).

While the first case of the West Nile Virus dates back to 1937 in the West Nile district of Uganda, its first occurrence in the United States wasn’t reported until the fall of 1999 (Sfakianos, and Hecht, 2009). Before that, however, there had been a few notable outbreaks in other parts of the globe. In 1957, an outbreak in Israeli nursing homes caused severe neurological disease and death (Center for Disease Control, 2007). The disease has increased in severity greatly since 1999, in which only 62 people with the disease were documented. In 2000, 21 people were reported infected and in 2001 66 people were reported infected. That number jumped to 4,156 people infected in 2002 and 9,862 in 2003 (Center for Disease Control, 2007). Of the number infected in 2003, 264 were killed by the disease (Klee, Maldin, Edwin, Poshni, Mostashari, Fine, Layton, and Nash, 2004). Investigations in during the 1999 West Nile virus outbreak in the United States revealed that older persons, and especially those with diabetes, were at an increased risk for contracting a severe West Nile virus disease (Klee, Maldin, Edwin, Poshni, Mostashari, Fine, Layton, and Nash, 2004). However it has been documented that prior to the 1990’s, the disease affected the young and healthy, showing that everyone is at risk for contracting the West Nile Virus (Center for Disease Control, 2007).

There are some obvious symptoms that persons infected with the virus may experience. These can include lethargy, headache, fever, general body ache and other flu like symptoms. In order to be diagnosed with West Nile virus, it is necessary to go to a doctor and have a blood sample taken. As “routine clinical laboratory studies do not distinguish WNV infection from many other viral infections (Hayes, Sejvar, Zaki, Lanciotti, Bode, and Campbell, 2005)”, it is necessary for in depth lab analysis to correctly diagnosis West Nile infection. West Nile virus can normally be detected by the presence of a West Nile virus specific immunoglobin blood serum within 8 days of the onset of the illness. Microsphere immunoassay are tests that can also detect the presence of the West Nile virus antibody in an infected patient (Hayes, Sejvar, Zaki, Lanciotti, Bode, and Campbell, 2005).

Despite the sharp decline in infected persons in the U.S. After 2004, there is still quite a bit of interest in continuing research on the West Nile virus and the development of a vaccine against it. Even though there is not currently a vaccine for the West Nile virus (Center for Disease Control, 2007) there are some precautions that can be taken to prevent contracting the virus. During the months when the disease is most active, August and September, it is wise to use insect repellent when going outdoors. Long sleeved protective clothing, mosquito netting while camping, and other item that protect against insect bites can help to limit mosquito bites and the possibility of contracting the virus.

The West Nile virus is an arbovirus, meaning that is passed to humans by an arthropod, a mosquito in the case of the WNV (Sfakianos, and Hecht, 2009). It is a virus that is in the family Flaviridae. The virus is shaped spherically, has a diameter of approximately 50 nanometers and is encased in a capsid. WNV contains a single strand of RNA that codes for 3 structural proteins and 7 non-structural proteins that, more than likely, contribute to the replication process. The three structural proteins coded for by the RNA of the WNV are the capsid (C), the envelope (E) and the premembrane (prM) (Hayes, Sejvar, Zaki, Lanciotti, Bode, and Campbell, 2005). While it is true that RNA virus populations are typically subject to high mutation rates, a study that compared the genetic structure of populations of WNV from 1999 to 2000 found a high level of consistency in the genetic material (Ebel, Dupuis, Ngo, Nicholas, Kauffman, Jones, Young, Maffei, Shi, Bernard, Kramer, 2001).  It is known that the WNV comes from two genetic lineages.  Lineage 1 strains are found in Australia, Africa, Asia, North America and Europe. The only two locations where Lineage 2 are found are in sub-Saharan Africa and Madagascar. Lineage one has been divided into four clades, the Kunjin, Indian, A and B.  Except for isolates in clade B, both lineages show both virulent and attenuated strains. Clade B isolates are all virulent. Through genetic analysis, it has been determined that the WNV strains found in the United States are almost identical to the ones from Israel, showing 99.7% homology in nucleotide sequences. This indicates with certainty that the strains in the U.S. originated in the Middle East (Hayes, Sejvar, Zaki, Lanciotti, Bode, and Campbell, 2005).

The WNV is believed to be spread by mosquito’s which pick it up when they bite an infected bird. Once a bird has been infected, the virus will flow freely through the birds bloodstream for 1 to 4 days. Infected mosquitoes then carry the virus in their salivary glands, where they can pass it to another bird species that next time they feed. The mosquito passes the infected bird blood to humans when it bites a person next (Center for Disease Control, 2007).  Black crows were the most commonly found bird species that was found dead from the WNV in 1999, just before the first human outbreak of the virus in New York (Sfakianos, and , Hecht 2009).

Once the WNV enters the bloodstream from the inoculation site, it moves to the lymph nodes. It makes its way through the blood-brain barrier by stimulating toll-like receptors to produce necrosis factor-?. This allows greater permeability of the blood-brain barrier (Hayes, Sejvar, Zaki, Lanciotti, Bode, and Campbell, 2005). Analysis of mice infected with WNV and showing signs of paralysis showed that the anterior horns of the spinal cords contained a high percentage of WNV infection. This indicates how WNV can lead to polio like symptoms, since the anterior horn of the spinal column is where the motor neurons reside (Shrestha, Gottlieb, and Diamond, 2003). Viral infection can directly injure the neural cells but they can also be damaged by “infiltrating leukocytes, inflammation cytokines, and activated microglial cells (Shrestha, Gottlieb, and Diamond, 2003).”

There have been other, non-mosquito modes of infection of the WNV in humans. Four cases of infection by organ transplants were reported in 2002. There have also been confirmed cases of infection via blood transfusions. Infants have become infected with the WNV while in the womb, being passed the virus by their mother. There has also been one probable case of an infant being infected with WNV through the mother’s breast-milk. In 2002, two lab workers were infected with WNV through contact at work (Center for Disease Control, 2007). Transmission of the virus by routes other than mosquito bites makes up a very small percentage of the total WNV infection cases.

Science has made great headway since the 1990’s in understanding the virology and pathology of the West Nile Virus. However, it is clear that more research needs to be done. In order to follow the disease and monitor its mutations, it is necessary to come up with a more practical and simple way to diagnose WNV in patients. More research on the natural history of WNV is needed in order to develop an effective treatment and therapies. Due to its potentially destructive and deadly nature, it may be necessary to develop a vaccine for the virus, especially for those who are at a higher risk for infection (Hayes, Sejvar, Zaki, Lanciotti, Bode, and Campbell, 2005). Though the incidence of West Nile virus has decreased since its peak in 2003 and 2004, it is still considered a menace that needs attention. RNA based viruses have been known to mutate wildly and rapidly, meaning that another large scale outbreak of the West Nile virus is possible in the future.

References

Center for Disease Control (November 14, 2007) West Nile Virus: Information and Guidance for  Clinicians.Retreived   October 4, 2010, from http://www.cdc.gov/ncidod/dvbid/westnile/clinicians/

Hayes, Edward B., Sejvar, James J., Zaki, Sherif R., Lanciotti, Robert S., Bode, Amy V., Campbell, Grant L. (August 2005). Virology, Pathology and Clinical Manifestations of the West Nile Virus Disease. Retrieved October 4, 2010 from http://www.cdc.gov/ncidod/EID/vol11no08/05-0289b.htm#cit

Hayes, Edward B., Komar, Nicholas, Nasci, Roger S., Montgomery, Susan P., O’Leary, Daniel R., Campbell, Grant L. (August 2005) Epidemiology and Transmission Dynamics of West Nile Virus Disease Retrieved October 4, 2010 from http://www.cdc.gov/ncidod/EID/vol11no08/05-0289a.htm

Klee, Anne Labowitz, Maldin, Beth, Edwin, Barbara, Poshni, Iqbal, Fine, Annie, Layton, Marcelle, Nash, Denis. (August 2004) Long Term Prognosis for Clinical West Nile Virus Infection Retrieved October 4, 2010 from http://www.cdc.gov/ncidod/Eid/vol10no8/03-0879.htm#table3

Marr, John S., Calisher, Charles H. (December 2003) Alexander the Great and West Nile Virus Encephalitis Retrieved October 4, 2010 from http://www.cdc.gov/ncidod/EID/vol9no12/03-0288.htm#Figure

Ebel, Gregory D., Dupuis, Alan P. III, Ngo, Kiet, Nicholas, David, Kauffman, Elizabeth, Jones, Susan A., Young, Donna, Maffei, Hoseph, Shi, Pei-Yong, Bernard, Kristen, Kramer, Laura D. (2001) Emerging Infectious Diseases, 7(4) http://www.cdc.gov/ncidod/EID/vol7no4/pdfs/v7n4.pdf

Sfakianos, Jeffrey N. and Hecht, Alan. (2009) West Nile Virus New York: Infobase Publishing

Shrestha, Bimmi, Gottlieb, David, Diamond, Michael S. (2003) Infection and Injury of Neurons by West Nile Encephalitis Virus. Journal of Virology, 77(24) http://jvi.asm.org/cgi/reprint/77/24/13203?maxtoshow=&hits=10&RESULTFORMAT=&fulltext=west+nile+fever&searchid=1&FIRSTINDEX=30&resourcetype=HWCIT