“1 And I heard a great voice out of the temple saying to the seven angels, Go your ways, and pour out the vials of the wrath of God upon the earth. 2 And the first went, and poured out his vial upon the earth; and there fell a noisome and grievous sore upon the men which had the mark of the beast, and upon them which worshiped his image.” – Revelation 16: 1-2
The first that happened was SARS (Severe Acute Respiratory Syndrome) which started in Guandong, China on November 16, 2002. In REVELATION 16:2 we read: “THE FIRST ANGEL WENT AND POURED OUT HIS BOWL ON THE EARTH. TERRIBLE AND PAINFUL SORES APPEARED ON THOSE WHO HAD THE MARK OF THE BEAST AND ON THOSE WHO HAD WORSHIPED ITS IMAGE”. In Guandong, China the people worship the image of the dragon. According to the Holy Bible, dragon is a beast and the first plague was poured out in China. The victims suffered from stinging pain and abominable wounds. The wound appeared in the human lungs and is known as SARS or CORONA VIRUS. Why is the pain so smarting? Human lungs is likened to a balloon. Once a person inhales the lungs expand and become smaller on exhalation. A person hit by SARS feels almost unbearable pain in the back in the process of inhalation and exhalation. The SARS victim prefers not to breath owing to severe pain in the lungs. Why is the wound abominable? People in the places with SARS wear face masks to avoid being afflicted by this sickness. This sickness spread throughout China, Taiwan, Hongkong, Singapore, Canada, and Vietnam. In the Philippines, few people became sick of SARS.
What is SARS?
SARS is a viral disease caused by a coronavirus, a subset group of viruses that are responsible for many cases of the “common cold”. Though the exact origins of this relatively new virus are unknown, it is believed that civets, a mammal with a cat-like appearance, may have been the source of transmission to humans.
In the Chinese province of Guangdong where the outbreak began, civets are considered a delicacy. A similar virus to SARS has also been discovered in Horseshoe bats, giving rise to the possibility that the bats transferred the virus to civets which in turn infected humans. In 2004, the sale of civets in the Guangdong province was banned and it was ordered that all civets in captivity should be slaughtered.
History of SARS and the 2003 Outbreak
It is believed that the disease was initially transferred to humans through civets, a mammal with a cat-like appearance. The SARS outbreak actually began in November 2002 in the Guangdong province of mainland China. However, to preserve public confidence, the Chinese government did not inform the World Health Organization (WHO) of the outbreak until February 2003.
How is SARS transmitted?
Though we are still in the process of trying to understand exactly how SARS is transmitted between humans, it is generally believed that the most common mode of transmission is through water droplets generated when an infected person coughs or sneezes.
This means that transmission is most likely to occur in close proximity to someone who is infected or by touching a surface where these water droplets have fallen, like a countertop. Current research indicates that SARS is not transmitted through the air except in very close proximity; the water droplets will quickly fall to the floor or other surfaces when they are sneezed or coughed up and do not remain suspended.
Symptoms of SARS
Initial symptoms are flu-like and include cough, fever, and sore throat. SARS can cause pneumonia and is fatal in some patients. In the 2003 outbreak, slightly less than 10% of believed SARS cases resulted in death. The only common symptom to all SARS patients is a fever of above 38°C.
SARS: Timeline of an Outbreak
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Main article: Severe acute respiratory syndrome
SARS, or Severe acute respiratory syndrome, is the disease caused by SARS coronavirus. It causes an often severe illness marked initially by systemic symptoms of muscle pain, headache, and fever, followed in 2–10 days by the onset of respiratory symptoms, mainly cough, dyspnea, and pneumonia. Another common finding in SARS patients is a decrease in the number of lymphocytes circulating in the blood.
In the SARS outbreak of 2003, about 9% of patients with confirmed SARS infection died. The mortality rate was much higher for those over 50 years old, with mortality rates approaching 50% for this subset of patients.
SARS coronavirus is a positive and single stranded RNA virus belonging to a family of enveloped coronaviruses. Its genome is about 29.7kb, which is one of the largest among RNA viruses. The SARS virus has 13 known genes and 14 known proteins. There are 265 nucleotides in the 5’UTR and 342 nucleotides in the 3’UTR. SARS is similar to other coronaviruses in that its genome expression starts with translation of two large ORFs 1a and 1b, which are two polyproteins.
The functions of several of these proteins are known: ORFs 1a and 1b encode the replicase and there are four major structural proteins: nucleocapsid, spike, membrane and envelope. It also encodes for eight unique proteins, known as the accessory proteins, with no known homologues. The function of these accessory proteins remains unknown.
Coronaviruses usually express pp1a (the ORF1a polyprotein) and the PP1ab polyprotein with joins ORF1a and ORF1b. The polyproteins are then processed by enzymes that are encoded by ORF1a. Product proteins from the processing includes various replicative enzymes such as RNA dependent polymerase, RNA helicase, and proteinase. The replication complex in coronavirus is also responsible for the synthesis of various mRNAs downstream of ORF 1b, which are structural and accessory proteins. Two different proteins, 3CLpro and PL2pro, cleave the large polyproteins into 16 smaller subunits.
SARS-Coronavirus follows the replication strategy typical of the Coronavirus genus.
The morphology of the SARS coronavirus is characteristic of the coronavirus family as a whole. These viruses have large pleomorphic spherical particles with bulbous surface projections that form a corona around particles. The envelope of the virus contains lipid and appears to consist of a distinct pair of electron dense shells.
The internal component of the shell is a single-stranded helical ribonucleoprotein. There are also long surface projections that protrude from the lipid envelop. The size of these particles are about 80–90 nm.
Coronavirus (CoV) genome replication takes place in the cytoplasm in a membrane-protected microenvironment and starts with the translation of the genome to produce the viral replicase. CoV transcription involves a discontinuous RNA synthesis during the extension of a negative copy of the subgenomic mRNAs. The requirement for base pairing during transcription has been formally demonstrated in arteriviruses and CoVs. The CoV N protein is required for coronavirus RNA synthesis and has RNA chaperon activity that may be involved in template switch. Both viral and cellular proteins are required for replication and transcription. CoVs initiate translation by cap-dependent and cap-independent mechanisms. Cell macromolecular synthesis may be controlled after CoV infection by locating some virus proteins in the host cell nucleus. Infection by different coronaviruses cause in the host alteration in the transcription and translation patterns, in the cell cycle, the cytoskeleton, apoptosis and coagulation pathways, inflammation and stress responses. The balance between genes up- and down-regulated could explain the pathogenesis caused by these viruses. Coronavirus expression systems based on single genome constructed by targeted recombination, or by using infectious cDNAs, have been developed. The possibility of expressing different genes under the control of transcription regulating sequences (TRSs) with programmable strength and engineering tissue and species tropism indicates that CoV vectors are flexible. CoV based vectors have emerged with high potential vaccine development and possibly for gene therapy.
SARS is most closely related to group 2 coronaviruses, but it does not segregate into any of the other three groups of coronaviruses. The closest outgroup to the coronaviruses are the toroviruses, with which it has homology in the ORF 1b replicase and the two viron proteins of S and M. SARS was determined to be an early split off from the group 2 coronaviruses based on a set of conserved domains that it shares with group 2.
A main difference between group 2 coronavirus and SARS is the nsp3 replicase subunit encoded by ORF1a. SARS does not have a papain-like proteinase 1.
Symptoms and treatment
Once a person has contracted SARS, the first symptom that they present with is a fever of at least 38°C (100.4°F) or higher. The early symptoms last about 2–7 days and include non-specific flu-like symptoms, including chills/rigor, muscle aches, headaches, diarrhea, sore throat, runny nose, malaise, and myalgia (muscle pain). Next, they develop a dry cough, shortness of breath, and an upper respiratory tract infection.
At that time, a chest x-ray is ordered to confirm pneumonia. If the chest appears clear and SARS is still suspected, a HRCT scan will be ordered, because it is visible earlier on this scan. In severe cases, it develops into respiratory failure and acute respiratory distress syndrome (ARDS), and in 70-90% of the cases, they develop lymphopenia (low count of lymphocyte white blood cells).
The incubation period for SARS-CoV is from 2–10 days, sometimes lasting up to 13 days, with a mean of 5 days. So symptoms usually develop between 2–10 days following infection by the virus. As part of the immune response, IgM antibody to the SARS-CoV is produced. This peaks during the acute or early convalescent phase (week 3) and declines by week 12. IgG antibody is produced later and peaks at week 12.