Severe acute respiratory syndrome is a life threatening condition that is caused by a virus from the Coronaviridae family. The SARS virus is believed to have originated from the Guangdong province of southern China before spreading to Hong Kong, Canada and the United States of America. The virus has an incubation period of 2 to 7 days but it may last up to 10 days. Like other respiratory disease, SARS is spread through direct contact; long range and short range. The major agent of transmission is the droplet nuclei. The symptoms of the disease include: fever, chills, malaise, cough, dyspnea and shortness of breath. The illness caused by the virus can be mild or extremely severe therefore resulting in death. The virus can be fatal as seen in China where the 2003 outbreaks resulted in 206 deaths. The outbreak in 2003 resulted in 8000 cases of infection of which 774 were fatal. The mortality rates as a result of infection with the SARS virus are highly variable. Older people are more prone to dying as a result of SARS as compared to younger people. According to the World Health Organization, the death rate among older people is more than 50%.
Some of the traits that result in the severity of the disease are: to begin with, the SARS virus posses five major open reading frames (ORFs) which are responsible for coding for replicase polyprotein. These ORFs are: the membrane glycoprotein (M), the envelope (E), the spike (S) and the nucleocapsid protein. The S protein contributes to the virulence of the virus. The S protein binds to specific host cell receptors therefore initiating the fusion between the envelope of the virus and the membrane of the cell. Much of the initial infection of the host by the virus is dependent on the interactions that are mediated by the spike protein. In most instances, the host cell is normally a ciliated epithelial respiratory cell found in the nasopharynx. In addition to that, the spike protein carries out antigenic functions by neutralization of the antibodies that are produced by the host.
The SARS virus has been found to highly stable and resistant. At room temperature, the virus remains viable in faeces and urine for a period of between 1 and 2 days. In diarrhea (which has a higher pH than normal stool), the virus can remain stable for up to 4 days. This stability accounts for the rapid spread of the virus in China especially among health workers who often have to handle stool samples in the course of their duties. In Amoy Gardens in Hong Kong, a sudden surge of cases of infection with the virus was attributed to sewage contamination. The contamination results in about 320 cases of infection. The doses that are necessary for the transmission of the virus via the faecal route are not yet known. Majority of the infections occur via person to person contact. In Hong Kong and China which were the epicenters of the 2003 outbreak, overcrowding and poor ventilation are thought to have significantly contributed to the spread of the virus. The SARS virus is a singled stranded ribonucleic acid and lacks an inherent mechanism of proofreading during replication of the RNA sequence. As a result, mutations of the RNA sequence often occur resulting in other forms of viruses that may prove to be more severe. Therefore when the virus spreads from one person to another, the form of RNA contracted by the other party may be more severe. This makes it difficult to treat the disease given that the emerging mutant forms may be resistant to the existing forms of therapy.
The SARS virus has evolved mechanisms of evading immune response. Type 1 interferon system possesses antiviral activity which is necessary for inhibiting the spread of the virus within the body. The SARS virus has mechanisms that protect it from being recognized by the Type 1 interferon system. Replication of the virus takes place within the cytoplasm. During replication, the virus remains enclosed by a double membrane. This enclosure results in separation of viral pathogen associated patterns and cellular cytoplasmic pattern recognition receptors. In order to prevent activation of the interferon system, there are 5 known SARS proteins which are responsible for inhibition in interferon regulatory factor 3. The interferon system can also be inducted through the gradual degradation of the host specific mRNA. These measures protect the SARS virus from being attacked by antiviral interferon system therefore exacerbating the spread and the severity of the virus. It is speculated that the strong adaptive and innate immune responses as a result of SARS virus are responsible for the severity of the disease. However, the exact mechanism is not fully understood hence the need for further research into the matter. Understanding this mechanism has the potential of providing information that would aid in the early diagnosis of SARS in addition to the development of a specific form of therapy.
Most significant trait
In my opinion, the most significant trait of the virus is its ability to evade the host’s immune response. This trait enables the virus to replicate fast and spread within the body and subsequently from one person to another. As a result, a person with the virus in the incubation period may easily spread it to another person given that the virus resists the antiviral responses mounted by the immune system. This takes place through several mechanisms: to begin with, the S protein possesses antiviral properties that protect the virus from the immune system during the initial infection of the host’s cells. In addition to this, during the replication of the virus, the virus remains enclosed within a double membrane and the replication takes place within the cytoplasm. The SARS virus also has proteins that inhibit interferon regulatory factor 3. By evading the immune system, the SARS virus is able to rapidly replicate and severely affect the host.
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