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Severe acute respiratory syndrome (SARS) is a serious type of pneumonia brought about by a virus that was initially recognized in 2003. The Spike protein (S) is among of the four leading structural proteins present in SARS Associated Coronavirus. This paper seeks to explore the structure and point of entry of SARS virus.
Severe acute respiratory syndrome (SARS) is a serious type of pneumonia brought about by a virus that was initially recognized in 2003. SARS virus infection results to acute respiratory distress and in worse cases, this can lead to death.
Dr. Carlo Urbani of the World Health Organization recognized SARS in 2003 when he examined a businessman who traveled from China through Hong Kong and to Vietnam. Both the businessman and the doctor passed away from SARS. As rapid as its appearance, the virus also spread quickly. This has affected people in Asia, Europe, Australia, Africa, South America, and North America. Several schools in Singapore and Hong Kong closed. The World Health Organization recognized SARS as a threat to global health. The fast worldwide public health reaction assisted in stemming the spread of SARS. SARS is a result of the spread of the coronavirus.
The Spike protein (S) is among of the four leading structural proteins present in SARS Associated Coronavirus ( 2013). S proteins are integrated to the viral envelope. This protein contains 1255 amino acids. Because of the low resemblance of amino acid series, this postulates that S protein of SARS-CoV has added functions aside from the usual functions. The carboxyl terminus is made up of the transmembrane region as well as the cytoplasmic tail. The tail is cysteine rich. The transmembrane area and cytoplasmic tail are merely 52 amino acids long. The extracellular area of the Spike protein is made up of two heptad areas ( 2013). These areas are known as HR1 or the heptad repeat region 1 and HR2 or the heptad repeat region 2, or HR-N as well as HR-C to signify the nearby terminus to the heptad region. HR1 and HR2 are divided by 140 amino acids known as the interhelical domain ( 2013). The two heptad regions can create a six helix bundle made up of three helices from heptad repeat region 1 that run anti-parallel to three helices from heptad repeat region 2.
An individual infected with SARS-CoV can activate a number of cellular and humoral immune responses (Lanying Du 2009). Certain antibodies in opposition to SARS-CoV (immunoglobulin G (IgG) and IgM) were noticeable just about 2 weeks after-infection, attaining a max out of 60 days post-infection and lingering at greater levels until 180 days after-infection. Greater titers of balancing antibodies as well as SARS-CoV-specific cytotoxic T lymphocyte reactions were perceived in individuals who had recuperated from SARS, and the quantity of the reactions associated well with the result of the disease outcome (Lanying Du 2009). This postulates that both cellular and humoral immune reactions are critical for the eradication of infection by SARS-CoV (Lanying Du 2009).
Coronavirus (CoV) genome duplication happens in the cytoplasm in a microenvironment protected by a membrane and begins with the conversion of the genome to generate the viral replicase ( 2013). Transcription of CoV encompasses an irregular RNA amalgamation during the expansion of a depressing duplicate of the subgenomic mRNAs. The prerequisite for base pairing that happens during transcription has been demonstrated in CoVs and antivirus ( 2013). The CoV N protein is needed for coronavirus RNA production and possessed RNA chaperon undertaking that may be implicated in pattern switch. Both cellular and viral proteins are needed for replication as well as transcription. CoVs start conversion by cap-dependent as well as cap-independent devices ( 2013). Cell macromolecular production may be organized following CoV infection by finding a number of virus proteins in the cell nucleus of the host. Infection by varied coronavirus results to the host adjustment in the transcription and patterns of translation, in the cytoskeleton, the cell cycle, coagulation pathways, apoptosis, stress responses, and inflammation ( 2013). The sense of balance amid genes could elucidate the pathogenesis brought about by these viruses. Coronavirus appearance grounded on single genome established by targeted recombination, or through the use of infectious cDNAs has been created. The potentiality of articulating varied genes under the power of TRSs or transcription regulating sequences with programmable potency and engineering tissue as well as species tropism signifies that there are flexible CoV vectors ( 2013).
SARS has taken the lives of over 770 individuals and contaminated over 8,000 globally since its appearance in southern China in 2002. Four other cases of possible SARS were documented in the UK.
SARS is mainly conveyed through contact with an infected person that leads to the deposition of respiratory droplets containing the virus on the mucous membranes of the nose, mouth, eyes. The particles of coronavirus present in these droplets will attack epithelial cells of the mucosal lining. The immune system struggles to drive away viral infection through the use of nonspecific immune defenses such as fever and inflammation, which aspire to restrict and control the spread of the virus, and antigen specific immune reactions (antibodies, T-cells). The objective of the immune reaction is to eradicate the virus as well as cells that harbor the virus. In the attempt to eradicate the origin of new virus, cell mediated immunity (T-cells) will kill the contaminated host cells. Thus, not only does the SARS virus stimulate the toxic impacts of host cell death, nevertheless the immune reaction provoked by the host can likewise produce toxic effects.
Similar to other respiratory diseases, SARS appears to be spread through contact with an infected person. For instance, an individual that is infected with SARS could sneeze or cough, thereby contaminating the surrounding immediately close to it through tiny droplets of matter that carries the infection. An individual close to the location where the virus is circulating can catch the air and breathe the virus. Due to the cause of SARS virus infection, experts are still taking into account other forms of contamination routes.
References (2013). Structure and Function of SARS-CoV S protein. [online] Retrieved from: [Accessed: 8 Dec 2013]. (2013). SARS: Sites of Toxicity. [online] Retrieved from: [Accessed: 8 Dec 2013].
Lanying Du, S. (2009). The spike protein of SARS-CoV — a target for vaccine and therapeutic development. Nature reviews. Microbiology, 7 (3), 226. doi:10.1038/nrmicro2090. (2013). Severe acute respiratory syndrome (SARS): MedlinePlus Medical Encyclopedia. [online] Retrieved from: [Accessed: 8 Dec 2013].