Coronavirus- An Overview

Coronaviruses are a large group of viruses that can infect humans and animals. They are named after the crown-like spikes that protrude from their surface, which are called spike (S) proteins. These proteins are responsible for attaching to and entering host cells.

Coronaviruses belong to the family Coronaviridae, which is divided into four genera: alpha, beta, gamma, and delta. Human coronaviruses (HCoVs) are mainly classified into alpha and beta genera. Some examples of HCoVs are 229E, NL63, OC43, HKU1, SARS-CoV, MERS-CoV, and SARS-CoV-2.

Coronaviruses have a spherical shape and a diameter of about 120 to 160 nanometers. They have an envelope made of a lipid bilayer that surrounds a nucleocapsid. The nucleocapsid is a helical structure that contains the viral genome and a protein called nucleocapsid (N) protein.

The viral genome is a single-stranded positive-sense RNA molecule that ranges from 27 to 32 kilobases in length. It encodes several proteins that are involved in viral replication, transcription, and assembly. The most important ones are the replicase gene products, which form a complex that synthesizes new viral RNA molecules.

The viral envelope also contains two other proteins: membrane (M) protein and envelope (E) protein. The M protein is the most abundant one and serves as a matrix that supports the shape of the virus and interacts with the nucleocapsid. The E protein is a small protein that plays a role in virus assembly and release.

Some coronaviruses, such as OC43 and HKU1, have a fourth protein on their envelope called hemagglutinin-esterase (HE) protein. This protein has two functions: it binds to sialic acid receptors on host cells and it cleaves ester bonds on the surface of host cells.

The structure of coronaviruses is important for understanding how they infect and cause disease in humans. The S protein determines the tropism and specificity of the virus for different cell types and organs. The N protein protects the viral RNA from degradation and regulates its transcription. The M and E proteins facilitate the assembly and release of new virions. The HE protein enhances the attachment and entry of some coronaviruses into host cells.

Coronavirus genomes are monopartite, single-stranded, positive-sense, polyadenylated, and capped RNAs ranging from 27 to 32 kb in length. They are among the largest known RNA genomes and have a complex organization and expression strategy. The 5′ approximately 20 to 22 kb carries the replicase gene, which encodes multiple enzymatic activities that are essential for viral replication and transcription. The replicase gene products are encoded within two very large open reading frames (ORFs), ORFs 1a and 1b, that span two-thirds of the genome. ORF1a is translated directly from the genomic RNA, while ORF1b is translated from a -1 ribosomal frameshift that occurs near the end of ORF1a. The resulting polyproteins are cleaved by viral proteases to generate 16 nonstructural proteins (nsps) that form the replication-transcription complex (RTC) in association with cellular membranes.

The 3′ one-third of the genome encodes the four common structural proteins: the spike (S), envelope (E), membrane (M), and nucleocapsid (N) proteins. The S protein is a large glycoprotein that forms the petal-shaped peplomers on the viral surface and mediates receptor binding and membrane fusion. The E protein is a small membrane protein that plays a role in virus assembly and release. The M protein is the most abundant structural protein that serves as a matrix protein embedded in the envelope lipid bilayer and interacting with the nucleocapsid. The N protein binds to the genomic RNA and forms the helical nucleocapsid. In addition to these four structural proteins, coronavirus genomes also include a variety of accessory ORFs that encode two to four nonstructural proteins of unknown functions. These accessory proteins may modulate host immune responses, viral pathogenesis, or tissue tropism.

The coronavirus genome has a 5′ cap structure and a 3′ poly(A) tail that facilitate its recognition by the host translation machinery. The genome also has a leader sequence at the 5′ end and a trailer sequence at the 3′ end that are involved in viral RNA synthesis. In between these sequences, there are conserved motifs such as the transcription-regulating sequence (TRS) and the packaging signal that regulate viral transcription and assembly. The TRS consists of a short conserved core sequence (CS) followed by a variable bulged stem-loop structure (BSL) that is present at the 5′ end of each gene and serves as a template switch site for discontinuous transcription of subgenomic RNAs. The packaging signal is a complex RNA structure that spans several kilobases near the 5′ end of the genome and interacts with the N protein to ensure specific encapsidation of the genomic RNA.

Coronavirus-infected cells contain multiple overlapping subgenomic, capped, and polyadenylated mRNAs with a common 3′ end. These mRNAs are synthesized by a process called discontinuous transcription, in which the RTC jumps from one TRS to another during negative-strand synthesis, resulting in a nested set of subgenomic RNAs with different lengths and leader-body junctions. Each subgenomic mRNA and the viral genomic RNA, which also serves as an mRNA, is translated to yield only the protein encoded by the 5′ gene on the mRNA. This is achieved by leaky scanning or ribosomal shunting mechanisms that bypass the upstream ORFs on the same mRNA. Thus, coronavirus genomes have a modular design that allows for differential expression of viral genes and generation of genetic diversity.

Coronaviruses are a large family of viruses that can cause respiratory, enteric, hepatic, and neurological diseases in humans and animals. The name coronavirus derives from the Latin corona, meaning crown or halo, which refers to the characteristic appearance of the virus particles under electron microscopy. There are four genera of coronaviruses: alpha, beta, gamma, and delta. Human coronaviruses belong to the alpha and beta genera.

The first human coronavirus (HCoV) was isolated in 1965 from a patient with a common cold. Since then, six more HCoVs have been identified: HCoV-229E, HCoV-OC43, HCoV-NL63, HCoV-HKU1, severe acute respiratory syndrome coronavirus (SARS-CoV), and Middle East respiratory syndrome coronavirus (MERS-CoV). The most recent HCoV to emerge is the novel coronavirus SARS-CoV-2, which causes coronavirus disease 2019 (COVID-19).

The epidemiology of HCoVs varies depending on the virus type, the host population, and the environmental factors. Most HCoVs cause mild to moderate upper respiratory tract infections that are self-limiting and have a seasonal pattern. However, some HCoVs can cause severe lower respiratory tract infections that can lead to pneumonia, acute respiratory distress syndrome (ARDS), and death. These include SARS-CoV, MERS-CoV, and SARS-CoV-2.

SARS-CoV was first detected in China in 2002 and caused a global outbreak of SARS in 2003, affecting 26 countries and resulting in 8,096 cases and 774 deaths. The main mode of transmission was through close contact with symptomatic patients or their respiratory secretions. The outbreak was contained by implementing strict infection control measures and contact tracing. No cases of SARS have been reported since 2004.

MERS-CoV was first detected in Saudi Arabia in 2012 and has caused sporadic outbreaks of MERS in the Middle East and other regions. As of May 2023, there have been 2,574 confirmed cases and 886 deaths reported to the World Health Organization (WHO). The main mode of transmission is through direct or indirect contact with dromedary camels or their products, which are considered the primary reservoir of the virus. Human-to-human transmission can also occur through close contact with infected patients or their respiratory secretions.

SARS-CoV-2 was first detected in China in late 2019 and has caused a global pandemic of COVID-19 since early 2020. As of May 2023, there have been 766,895,075 confirmed cases and 6,935,889 deaths reported to WHO. The main mode of transmission is through respiratory droplets or aerosols that are generated when an infected person coughs, sneezes, or talks. The virus can also spread through contact with contaminated surfaces or objects. The incubation period ranges from 1 to 14 days, with a median of 5 days. The symptoms include fever, cough, shortness of breath, loss of taste or smell, and other manifestations. Some people may develop severe complications such as pneumonia, ARDS, septic shock, multiorgan failure, or death.

The epidemiology of COVID-19 is dynamic and evolving as new variants of SARS-CoV-2 emerge and spread around the world. These variants may have different characteristics such as transmissibility, virulence, immune escape, or vaccine efficacy. CDC uses genomic surveillance to track the spread of variants and monitor their impact on public health.

The prevention and control of HCoVs depend on the availability and effectiveness of vaccines, antivirals, diagnostics, and public health measures. CDC provides guidance and resources for different risk groups and settings to reduce the transmission and impact of HCoVs.

Coronaviruses replicate in the cytoplasm of host cells using their positive-sense RNA genome as a template for both transcription and translation. The replication cycle of coronaviruses can be summarized as follows:

• Attachment and entry: Coronaviruses attach to their glycoprotein receptors on host cells via their spike (S) proteins. Viral entry is mediated by fusion of the viral envelope with the host cell membrane or by receptor-mediated endocytosis. The fusion of the viral and cell membranes is facilitated by the S2 portion of the virus spike protein, which functions as a class 1 fusion protein. Once the viral RNA is released into the cytoplasm, it is translated to produce a large polyprotein that undergoes proteolytic processing to generate an RNA-dependent RNA polymerase (RdRp).
• Replication and transcription: The RdRp translated from the plus-stranded viral genomic RNA makes a negative-strand that serves as the template for a nested set of five to seven subgenomic mRNAs. Each subgenomic mRNA and the viral genomic RNA, which also serves as an mRNA, is translated to yield only the protein encoded by the 5′ gene on the mRNA. The subgenomic mRNAs are synthesized by a discontinuous transcription mechanism that involves leader-body fusion. A common intergenic sequence (IS) of about 7 bases is found at the 5′ end of each gene, which is essential for the formation of subgenomic RNAs.
• Assembly and release: The nucleocapsid (N) protein and newly synthesized genomic RNA associate to form helical nucleocapsids. The membrane (M) glycoprotein is inserted in the endoplasmic reticulum (ER) and anchored in the Golgi apparatus. The nucleocapsid binds to M protein at the budding compartment (ERGIC). The envelope (E) and spike (S) proteins interact with M protein to trigger the budding of virions, enclosing the nucleocapsid. Some viruses, such as human coronavirus OC43 (HCoV-OC43), also contain a hemagglutinin-esterase (HE) glycoprotein that causes hemagglutination and has acetylesterase activity. These newly formed virions are transported via the Golgi apparatus to the plasma membrane where they are released by exocytosis.

The pathogenesis of coronavirus refers to the mechanisms by which the virus causes disease in the host. Coronavirus infection can result in a range of clinical outcomes, from asymptomatic or mild respiratory illness to severe pneumonia and multi-organ failure. The factors that determine the severity and progression of disease are not fully understood, but they may include viral factors (such as viral load, strain, and mutations), host factors (such as age, sex, comorbidities, and genetic susceptibility), and environmental factors (such as exposure dose and route).

The primary route of transmission of human coronaviruses is via the respiratory tract, through inhalation of aerosols or droplets containing the virus. The virus can also be transmitted through contact with contaminated surfaces or fomites. The virus attaches to its receptors on the host cells via its spike (S) glycoprotein, which mediates fusion of the viral envelope with the cell membrane or endocytosis of the virus into the cell. The main receptor for SARS-CoV-2 is angiotensin-converting enzyme 2 (ACE2), which is expressed on various cell types in the respiratory tract, such as alveolar epithelial cells, ciliated cells, goblet cells, and type II pneumocytes . Other receptors or co-receptors that may facilitate viral entry include neuropilin-1, CD147, and heparan sulfate.

Once inside the cell, the virus releases its genomic RNA into the cytoplasm, where it is translated into two large polyproteins that are cleaved by viral proteases into non-structural proteins (NSPs). The NSPs form a replication-transcription complex (RTC) that synthesizes new viral RNA using the negative-strand RNA as a template. The RTC also produces a set of subgenomic RNAs that encode the structural proteins (S, E, M, and N) and accessory proteins. The structural proteins assemble with the genomic RNA to form new virions, which are transported to the cell surface and released by exocytosis or lysis .

The infection of respiratory epithelial cells by coronavirus can cause direct cytopathic effects, such as cell death, apoptosis, necrosis, or pyroptosis. The infection can also trigger an innate immune response, involving the recognition of viral RNA by pattern recognition receptors (PRRs), such as toll-like receptors (TLRs) and retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs). The activation of PRRs leads to the production of type I and III interferons (IFNs) and pro-inflammatory cytokines (such as interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and chemokines), which recruit and activate various immune cells, such as macrophages, dendritic cells, natural killer cells, and T cells .

The adaptive immune response to coronavirus infection involves both humoral and cellular immunity. The humoral immunity is mediated by B cells that produce virus-specific antibodies that can neutralize the virus or facilitate its opsonization and phagocytosis. The cellular immunity is mediated by T cells that can recognize viral antigens presented by major histocompatibility complex (MHC) molecules on infected cells or antigen-presenting cells. CD4+ T helper cells can secrete cytokines that regulate B cell activation and antibody production, as well as CD8+ cytotoxic T cell activation and proliferation. CD8+ cytotoxic T cells can kill infected cells by releasing perforin and granzymes or by inducing apoptosis through Fas-Fas ligand interaction .

The immune response to coronavirus infection can be protective or pathogenic depending on its magnitude and balance. A timely and adequate immune response can clear the virus and limit tissue damage. However, a delayed, insufficient, or excessive immune response can result in persistent viral replication, tissue injury, systemic inflammation, and immunopathology. Some of the mechanisms that may contribute to coronavirus-induced immunopathology include:

• Dysregulated cytokine production: Coronavirus infection can cause an excessive production of pro-inflammatory cytokines and chemokines by infected cells or immune cells, leading to a cytokine storm syndrome that can cause vascular leakage, organ dysfunction, shock, and death .
• Impaired interferon response: Coronavirus infection can interfere with the type I IFN response by various mechanisms, such as blocking IFN signaling pathways, degrading IFN-stimulated genes, inhibiting IFN production, or inducing IFN resistance. A reduced IFN response can impair viral clearance and enhance viral replication .
• Lymphocyte depletion: Coronavirus infection can cause lymphopenia, especially in severe cases . The causes of lymphopenia may include increased apoptosis, reduced proliferation, impaired trafficking, or direct infection of lymphocytes. Lymphopenia can impair both innate and adaptive immunity and increase susceptibility to secondary infections.
• Autoimmunity: Coronavirus infection can induce autoantibodies or autoreactive T cells that target self-antigens or cross-react with viral antigens. Autoimmunity can cause tissue damage or organ dysfunction in various systems .
• Immunological memory: Coronavirus infection can induce immunological memory that confers protection against reinfection or disease progression. However, immunological memory may also have negative consequences, such as antibody-dependent enhancement (ADE) or original antigenic sin (OAS). ADE occurs when non-neutralizing antibodies facilitate viral entry into Fc receptor-bearing cells . OAS occurs when pre-existing antibodies or memory T cells cross-react with a new viral strain but fail to neutralize it or elicit an optimal immune response .

The pathogenesis of coronavirus infection is influenced by multiple factors at different levels of biological organization. A better understanding of these factors may help to identify biomarkers for disease prognosis and targets for therapeutic intervention.

Coronaviruses can cause a variety of symptoms in humans, ranging from mild to severe. The most common symptoms of coronavirus disease 2019 (COVID-19), the disease caused by SARS-CoV-2, are :

• Fever or chills
• Cough
• Shortness of breath or difficulty breathing
• Fatigue
• Muscle or body aches
• Headache
• New loss of taste or smell
• Sore throat
• Congestion or runny nose
• Nausea or vomiting
• Diarrhea

These symptoms may appear 2 to 14 days after exposure to the virus. However, some people may have no symptoms at all (asymptomatic infection) or only mild symptoms that resemble a common cold. The severity of symptoms may vary depending on factors such as age, underlying medical conditions, immune status, and viral load.

Some people with COVID-19 may develop more serious complications, such as pneumonia, acute respiratory distress syndrome (ARDS), septic shock, multiorgan failure, blood clots, or death . These complications are more likely to occur in older adults, people with chronic diseases (such as heart disease, lung disease, diabetes, or kidney disease), people with weakened immune systems, and pregnant women .

Some people with COVID-19 may also experience symptoms that affect other organs or systems, such as :

• Skin rashes or discoloration of fingers or toes
• Conjunctivitis (pink eye)
• Inflammation of the heart muscle (myocarditis) or lining (pericarditis)
• Irregular heart rhythms (arrhythmias) or low blood pressure (hypotension)
• Blood vessel inflammation (vasculitis) or damage (endothelial dysfunction)
• Stroke or transient ischemic attack (TIA)
• Seizures or encephalopathy
• Guillain-Barré syndrome or other neurological disorders
• Loss of kidney function (acute kidney injury) or chronic kidney disease
• Liver injury or dysfunction
• Gastrointestinal symptoms such as abdominal pain, diarrhea, nausea, vomiting, or loss of appetite
• Secondary bacterial or fungal infections

Some people with COVID-19 may also have long-term effects that persist for weeks or months after recovery. These effects are collectively known as "long COVID" or "post-COVID syndrome" and may include :

• Fatigue
• Shortness of breath
• Cough
• Chest pain
• Joint pain
• Muscle pain
• Headache
• Memory loss or cognitive impairment ("brain fog")
• Depression, anxiety, or post-traumatic stress disorder (PTSD)
• Sleep problems
• Loss of smell or taste
• Tinnitus (ringing in the ears) or hearing loss
• Hair loss
• Menstrual irregularities

The exact causes and mechanisms of these long-term effects are not fully understood and may vary depending on the individual. More research is needed to understand the long-term consequences of COVID-19 and how to prevent and treat them.

The clinical manifestations of COVID-19 are diverse and evolving. Therefore, it is important to monitor the symptoms and seek medical attention if they worsen or become severe. Early diagnosis and treatment can help reduce the risk of complications and improve the outcomes of COVID-19.

Laboratory diagnosis of coronavirus infection is important for confirming the presence of the virus, monitoring the disease progression and severity, and evaluating the effectiveness of treatment and prevention measures. There are different types of tests available for detecting the coronavirus, depending on the purpose and the stage of infection.

Types of tests

The main types of tests for coronavirus are:

• Viral tests: These tests detect the genetic material or proteins of the virus that causes COVID-19 in respiratory specimens, such as nasal or throat swabs, or saliva samples. The most common and reliable viral test is the real-time reverse transcription polymerase chain reaction (RT-PCR) test, which amplifies and identifies specific viral RNA sequences. Other viral tests include antigen tests, which detect viral proteins on the surface of the virus, and loop-mediated isothermal amplification (LAMP) tests, which also amplify viral RNA but use a different technique than RT-PCR. Viral tests are used to diagnose active infection and determine the viral load and contagiousness of the patient. They are usually performed within the first week of symptoms or exposure to the virus.

• Antibody tests: These tests detect the presence of antibodies, which are proteins produced by the immune system in response to the virus, in blood samples. Antibody tests can indicate a past or recent infection, as well as the immune status and protection level of the patient. However, antibody tests cannot diagnose active infection, as antibodies take time to develop after exposure to the virus. They are usually performed after 10 days of symptoms or exposure to the virus.

• Other tests: These tests measure other biomarkers or indicators of infection or inflammation in blood or other body fluids, such as cytokines, C-reactive protein (CRP), D-dimer, ferritin, lactate dehydrogenase (LDH), procalcitonin, etc. These tests can help assess the severity and complications of COVID-19, such as cytokine storm, coagulopathy, organ damage, etc. They are usually performed in hospitalized patients with moderate to severe disease.

Testing procedures

The testing procedures for coronavirus vary depending on the type of test, the specimen collection method, and the laboratory setting. The general steps are:

• Specimen collection: A health care professional collects a sample from the patient using a nasal swab (nasopharyngeal swab), a throat swab (oropharyngeal swab), a saliva sample, or a blood sample. The specimen should be collected as soon as possible after the onset of symptoms or exposure to the virus. The specimen should be handled with care and transported to the laboratory under appropriate conditions to avoid contamination or degradation.

• Specimen processing: The laboratory technician prepares the specimen for testing by extracting the viral RNA or antibodies from it using specific reagents and protocols. The extracted material is then amplified or detected using different techniques depending on the type of test.

• Specimen analysis: The laboratory technician analyzes the results of the test by comparing them with positive and negative controls and interpreting them according to predefined criteria. The results are then reported to the health care provider and/or public health authorities.

Testing challenges

There are several challenges and limitations associated with laboratory diagnosis of coronavirus infection, such as:

• Accuracy: The accuracy of a test depends on its sensitivity (the ability to correctly identify positive cases) and specificity (the ability to correctly identify negative cases). No test is 100% accurate, and there is always a possibility of false positive or false negative results due to various factors, such as cross-reactivity with other viruses or bacteria, contamination or degradation of specimens or reagents, human errors, etc. Therefore, it is important to validate and evaluate each test before using it for clinical or public health purposes.

• Availability: The availability of a test depends on its cost, complexity, accessibility, and scalability. Some tests require specialized equipment, trained personnel, and adequate infrastructure that may not be available in all settings or regions. Some tests may also have limited supply or demand that may affect their availability. Therefore, it is important to prioritize and allocate testing resources according to the needs and capacities of each setting or region.

• Timeliness: The timeliness of a test depends on its turnaround time (the time between specimen collection and result reporting) and frequency (the number of times a test is performed on a patient or a population). Some tests may take longer than others to produce results due to various steps involved in specimen processing and analysis. Some tests may also need to be repeated at different intervals to monitor changes in infection status or immune response. Therefore, it is important to optimize and streamline testing workflows and protocols to ensure timely diagnosis and management of COVID-19 cases.

There is no specific cure for COVID-19, but there are some treatments that can help reduce the severity and duration of the illness. The treatment options depend on the severity of the symptoms, the risk factors for complications, and the availability of the medications.

Antiviral medications

The U.S. Food and Drug Administration (FDA) has approved one antiviral medication, remdesivir (Veklury), to treat COVID-19 in hospitalized adults and children who are age 12 and older. Remdesivir works by blocking a key enzyme that the virus needs to replicate. It is given through a vein (intravenously) over several days.

The FDA has also authorized two oral antiviral medications, Paxlovid and molnupiravir, to treat mild to moderate COVID-19 in people who are age 12 and older and who are at high risk for progression to severe COVID-19 . Paxlovid consists of two drugs, nirmatrelvir and ritonavir, that work together to inhibit the viral enzyme and prevent its breakdown. Molnupiravir works by introducing errors into the viral RNA, making it unable to replicate. Both medications are taken by mouth as pills and must be started within five days of symptom onset.

Antiviral medications are not effective for everyone and may have side effects. They should be prescribed by a health care provider and taken as directed.

Symptomatic relief

For mild symptoms of COVID-19, such as fever, cough, sore throat, or headache, over-the-counter medications such as acetaminophen (Tylenol) or ibuprofen (Advil) may help relieve the discomfort. However, these medications do not treat the underlying infection and should not be used for more than a few days without consulting a health care provider.

Other measures that may help with mild symptoms include:

• Drinking plenty of fluids to stay hydrated
• Resting as much as possible
• Using a humidifier or a warm shower to ease breathing
• Gargling with salt water or using lozenges to soothe a sore throat
• Avoiding smoking and alcohol

If symptoms worsen or do not improve within a week, seek medical attention.

Supportive care

For severe or critical cases of COVID-19 that require hospitalization, supportive care may include:

• Oxygen therapy to help with low blood oxygen levels
• Mechanical ventilation to assist with breathing
• Steroids to reduce inflammation
• Blood thinners to prevent blood clots
• Monoclonal antibodies to boost the immune response
• Extracorporeal membrane oxygenation (ECMO) to oxygenate the blood outside the body

Supportive care aims to stabilize the vital signs and prevent organ failure. The type and duration of supportive care depend on the individual condition and response to treatment.

Prevention

The best way to prevent COVID-19 is to get vaccinated against the virus. Vaccines are safe and effective at preventing severe illness and death from COVID-19. They also reduce the risk of transmission and infection by new variants.

Other preventive measures include:

• Wearing a mask or a face covering when in public or around people who are not from your household
• Practicing physical distancing by staying at least 6 feet (2 meters) away from others
• Washing your hands frequently with soap and water or using an alcohol-based hand sanitizer
• Avoiding touching your eyes, nose, or mouth with unwashed hands
• Covering your mouth and nose with a tissue or your elbow when you cough or sneeze
• Cleaning and disinfecting frequently touched surfaces
• Staying home if you are sick or have been exposed to someone with COVID-19
• Getting tested if you have symptoms or have been in close contact with someone who has COVID-19

By following these steps, you can protect yourself and others from COVID-19.

Coronavirus is a group of viruses that can cause respiratory infections, gastroenteritis, and neurological disorders in humans and animals. The most recent coronavirus outbreak, caused by the novel SARS-CoV-2 virus, has resulted in a global pandemic of COVID-19, a disease that can range from mild to severe and can lead to death in some cases.

COVID-19 can be prevented through pharmaceutical (i.e., vaccination) and non-pharmaceutical interventions (e.g., masking, physical distancing, hand hygiene). All of these preventative measures are important to protect individuals from acquiring and transmitting the SARS-CoV-2 virus and should be done in conjunction with one another.

Some of the prevention and control measures for coronavirus are:

• Staying up to date with COVID-19 vaccines: COVID-19 vaccines help the body develop protection from the virus that causes COVID-19. Although vaccinated people sometimes get infected with the virus that causes COVID-19, staying up to date on COVID-19 vaccines significantly lowers the risk of getting very sick, being hospitalized, or dying from COVID-19. CDC recommends that everyone stay up to date on their COVID-19 vaccines, especially people with weakened immune systems.

• Improving ventilation and spending time outdoors: Improving ventilation (moving air into, out of, or within a room) and filtration (trapping particles on a filter to remove them from the air) can help prevent virus particles from accumulating in indoor air. Improving ventilation and filtration can help protect you from getting infected with and spreading the virus that causes COVID-19. Spending time outside when possible instead of inside can also help: Viral particles spread between people more readily indoors than outdoors.

• Getting tested for COVID-19 if needed: Testing for COVID-19 can help identify people who are infected with the virus that causes COVID-19, even if they do not have symptoms or have mild symptoms. Testing can also help determine if someone has been exposed to the virus that causes COVID-19 and needs to quarantine or isolate. Testing can also help monitor the spread of the virus in communities and inform public health actions.

• Following recommendations for what to do if you have been exposed: If you have been in close contact with someone who has COVID-19, you should follow CDC`s guidance on what to do after exposure. Depending on your vaccination status, you may need to quarantine for a certain period of time, monitor your symptoms, get tested, and wear a mask around others.

• Staying home if you have suspected or confirmed COVID-19: If you have symptoms of COVID-19 or a positive test result, you should stay home and isolate yourself from others until you meet the criteria to end isolation. This will help prevent spreading the virus to others and protect your health. You should also notify your health care provider and follow their advice on treatment options.

• Seeking treatment if you have COVID-19 and are at high risk of getting very sick: Some people with COVID-19 may develop severe illness that requires hospitalization or intensive care. People who are older, have underlying medical conditions, or are immunocompromised are at higher risk of severe illness from COVID-19. If you have COVID-19 and are at high risk of getting very sick, you should seek medical attention as soon as possible and ask your health care provider about treatment options such as monoclonal antibodies or antiviral drugs.

• Avoiding contact with people who have suspected or confirmed COVID-19: If you know someone who has COVID-19 or has symptoms of COVID-19, you should avoid contact with them as much as possible. You should also avoid sharing personal items such as utensils, cups, towels, or bedding with them. If you need to care for someone who has COVID-19, you should wear a mask, gloves, and other personal protective equipment (PPE) as recommended by CDC.

• Wearing a face mask: A face mask is a simple but effective way to prevent the spread of respiratory droplets that may contain the virus that causes COVID-19. Wearing a mask can protect you from inhaling or exhaling these droplets and reduce the risk of infection for yourself and others. CDC recommends wearing a mask indoors in public settings where there is substantial or high transmission of COVID-19 in your community, regardless of your vaccination status. You should also wear a mask outdoors in crowded settings where physical distancing is difficult.

• Practicing good hand hygiene: Washing your hands often with soap and water for at least 20 seconds can help remove germs from your hands and prevent them from entering your body through your eyes, nose, or mouth. You should wash your hands before eating or preparing food, after using the bathroom, after coughing or sneezing, after touching public surfaces or objects, and after caring for someone who is sick. If soap and water are not available, you can use an alcohol-based hand sanitizer that contains at least 60% alcohol.

• Maintaining physical distance: Physical distance means keeping a safe space between yourself and other people who are not from your household. Physical distance can help reduce the chance of coming into contact with respiratory droplets that may contain the virus that causes COVID-19. CDC recommends staying at least 6 feet (2 meters) away from others who are not from your household in both indoor and outdoor settings.

By following these prevention and control measures for coronavirus, you can help protect yourself and others from getting sick and stop the spread of the virus in your community.

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