Category Archives: COVID-19

All Types of COVID-19 Vaccines, How They Work, with Animation.

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How it works. mRNA vaccine (Pfizer, Moderna), DNA & Viral vector vaccines (Johnson & Johnson (J&J, JNJ), Oxford-AstraZeneca, Inovio, Sputnik V); protein/peptide vaccine (Novavax, EpiVacCorona), conventional inactivated (CoronaVac of Sinovac, Covaxin). Mechanism of each type of coronavirus vaccines explained. Vaccine-induced immune response as compared to natural immunity.

During a natural viral infection, infected cells alert the immune system by displaying pieces of viral proteins on their surface. They are said to present the viral antigen to immune cells – cytotoxic T-cells, and activate them.
Debris of dead cells and viral particles are picked up by professional antigen-presenting cells, (dendritic cells…). Dendritic cells patrol body tissues, sampling their environment for intruders. After capturing the antigen, dendritic cells leave the tissue for the nearest lymph node, where they present the antigen to another group of immune cells – helper T-cells. Viral particles also activate B-cells.
These cells mount 2 types of immunity specific to the viral antigen: cell-mediated immunity and antibody-mediated immunity.
Vaccines deliver viral antigens to trigger immune responses without causing the disease. The events of a vaccine-induced immune response are similar to that induced by a natural infection, although some types of vaccines may induce only antibody-mediated immunity (B cell immunity, not T cell (cellular) immunity).
Many existing vaccines contain a weakened or an inactivated virus. Because the whole virus is used, these vaccines require extensive safety testing. Live attenuated vaccines may still cause disease in people with compromised immune systems. Inactivated vaccines (Sinovac/China, Covaxin/India) only induce humoral (B cell) immunity.
Subunit vaccines contain only part of the virus, usually a spike protein (peptide – EpiVacCorona/Russia). These vaccines may not be seen as a threat to the immune system, and therefore may not elicit the desired immune response. For this reason, certain substances, called adjuvants, are usually added to stimulate the antigen-presenting cells to pick up the vaccine.
Nucleic acid vaccines contain genetic information for making the viral antigen, instead of the antigen itself. Naked DNA vaccines (Inovio, phase 2/3 clinical trials) require a special delivery method to reach the cell’s nucleus (electroporation). Alternatively, a harmless, unrelated virus may be used as a vehicle to deliver the DNA. In this case, the vaccine is also known as viral-vector vaccine (Sputnik V/Russia, Oxford-AstraZeneca, Johnson & Johnson’s). For example, the Oxford-AstraZeneca Covid-19 vaccine uses a chimpanzee adenovirus as a vector. The adenoviral genome is modified to remove viral genes, and the coronavirus spike gene is added. This way, the viral vector cannot replicate or cause disease, but it acts as a vehicle to deliver the DNA. Why a non-human adenovirus is used?
Do DNA vaccines change human DNA?
mRNA vaccines (Pfizer, Moderna) are delivered within a lipid covering that will fuse with the cell membrane. The mRNA is translated into viral antigen, which is then displayed on the cell surface. mRNA vaccines are extremely unlikely to integrate into human genome.
All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition.

Cerebral Venous Sinus Thrombosis, CVST, with Animation

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CVST is a type of brain stroke caused by blood clots in a vein. This rare blood clot disorder prompted the current pause of Johnson & Johnson (J&J) COVID-19 vaccine, as well as Astrazeneca vaccine.

Pathophysiology, signs and symptoms, risk factors, diagnosis, treatment and prognosis.

Other names: Cerebral vein thrombosis, Cerebral sinovenous thrombosis, Cerebral venous thrombosis (CVT), Cerebral venous and sinus thrombosis, Cerebral venous sinus thrombosis (CVST), Cerebral sinovenous thrombosis (CSVT), Cerebral vein and dural sinus thrombosis, Sinus and cerebral vein thrombosis.

Cerebral venous sinus thrombosis, CVST, occurs when a blood clot forms and blocks a vein in the brain. Blood is transported to the brain in arteries. After delivering oxygen and nutrients, it leaves in veins. Small veins of the brain are called cerebral veins. They drain into large veins, called sinus veins, or venous sinuses. Sinus veins empty into jugular veins, which carry the blood back to the heart. A blockage in a vein causes the blood to back up in the brain, increasing pressure, causing headache, which is often severe. The increased pressure may damage the surrounding brain tissue, producing stroke symptoms such as blurred vision, confusion, loss of consciousness, loss of movement control, seizure or coma. The engorged blood vessel may also rupture, bleeding into the brain, a condition known as “venous hemorrhagic stroke”. Unlike arterial thrombosis that causes the typical brain stroke, venous thrombosis usually develops slowly. This is due to the slow growth of blood clots in veins, and the ability of the venous system to form new vessels to bypass an obstruction, maintaining more or less normal flow at first. In most cases, symptoms develop gradually, over days, weeks or even months, but sudden onset may also occur. CVST is a rare type of stroke that can affect all age groups, including infants. Risks factors include: having inherited blood disorders, systemic conditions, cancers; use of certain medications, and some infections. Women of reproductive age are more at risk due to pregnancy and use of birth control pills. Infants with difficult birth, or whose mothers had certain infections, are also more vulnerable. CVST is often misdiagnosed due to its rarity, wide spectrum of symptoms, and the fact that symptoms can appear suddenly or gradually. The standard MRI or CT scans used to detect stroke are often normal in CVST. To diagnose CVST, the veins must be specifically examined in a procedure called magnetic resonance venography. CVST must be suspected in patients of any age who have severe headache that doesn’t go away, and any risk factors for clotting disorders. Timely diagnosis and prompt treatments are essential for survival. Immediate treatment includes blood thinners, typically intravenous heparin, or subcutaneous low-molecular-weight heparin. The goal is to prevent the enlargement of existing clots and formation of new clots, while letting the body’s own system dissolves the existing clots slowly, typically over weeks or months. However, patients who have bleeding must be monitored closely to ensure it does not worsen. If the patient deteriorates despite heparin, catheter-directed procedures to breakdown blood clots may be considered. Once the patient is out of danger, an oral anticoagulant such as warfarin is typically given for 3 to 6 months, although patients with known clotting disorders may need to take warfarin for life. About 3 in 4 patients fully recover, but it may take some time to get back to normal.

COVID-19 Tests Explained

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There are 2 major types of COVID-19 tests: diagnostic tests for active infection, and antibody tests for past infection.
Diagnostic tests look for components of the virus in a sample taken from the nasal cavity, throat, or saliva. Sample taken from the nasopharynx, the upper part of the throat behind the nose, is preferred when higher accuracy is required.
There are 2 types of diagnostic tests: molecular tests detecting viral RNA, and antigen tests detecting viral proteins.
Antigen tests use a technology similar to that of a pregnancy test. Some are made available as at-home test kits. The test is fast and less expensive, but is less sensitive. Antigen test gives positive results only with high viral loads, when the person is near the peak of infection, so it’s more likely to miss an active infection. In other words, the rate of false negative – a test that says you don’t have the virus when you actually do, is high. Symptomatic patients who test negative with rapid antigen test must be confirmed with a more sensitive molecular test. On the other hand, positive results are highly accurate, but false positive – a test that says you have the virus when you actually don’t, can still happen, most commonly due to errors in sample handling.
Molecular tests detect viral RNA. They are also called nucleic acid amplification tests, NAAT, because they amplify viral nucleic acids until there are detectable levels. Different tests are based on different technologies, with polymerase chain reaction, PCR, being just one of them. PCR is the gold standard for diagnostic testing but it requires specific equipment and takes longer to deliver results.
Molecular tests are much more sensitive than rapid antigen tests, but they can still produce false-negative results early in the infection. On the other hand, the high sensitivity may sometimes pick up the low viral load in a patient who has recovered and is no longer contagious. Positive results are highly accurate, most false positives are due to lab contamination or other errors with sample handling.
Antibody tests, also called serology tests, detect antibodies that the body produced in response to the infection. A blood sample is taken for this test. Because antibodies can take a couple of weeks to develop and may stay in the blood for weeks or months after recovery, a positive test result only proves that the person has been exposed to the virus. It gives no indication about active infection and should not be used to diagnose COVID-19.

Current status of possible treatments for COVID-19, with Animation, updated May 1, 2020

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Convalescent plasma, Remdesivir, Chloroquine and hydroxychloroquine: mechanisms of action, current status, effectiveness and side effects.
At this time, no specific drugs or therapies have been proven effective for prevention or treatment of COVID-19. Current disease management is supportive care, including supplemental oxygen and mechanical ventilator when indicated.
However, several possible treatment options are under intensive investigations:
Convalescent plasma: when someone is infected with SARS-CoV-2, the coronavirus that causes COVID-19, their immune system produces antibodies to fight the virus. People with healthy immune systems produce enough antibodies to fight the disease and recover, while those with compromised immune systems may struggle. Antibodies from blood plasma of recovered patients can be given to people with active illness to help neutralize the virus. This approach has been used in the past for some other diseases, with varying success. Studies are underway to determine its effectiveness in COVID-19, and if convalescent plasma is best used to prevent infections in high-risk individuals; to prevent mild infections from becoming severe; or to improve recovery in severely ill patients. The FDA has allowed emergency use of convalescent plasma in patients with serious or immediately life-threatening COVID-19 infections. While the treatment concept is simple, the process involves multiple steps, from selecting donors, to collecting, processing blood and safety screening. On average, plasma from one donor is only enough to treat 1 to 3 patients. For these reasons, convalescent plasma is considered a temporary solution while antiviral drugs and vaccines are developed.
Remdesivir is an antiviral drug originally created by Gilead Sciences to fight Ebola virus, but it was proved effective in treating SARS and MERS coronaviruses in laboratory and animal research. Recent studies show that Remdesivir inhibits SARS-CoV-2 infections in cultured cells, and efficiently prevents COVID-19 disease progression in monkeys. Remdesivir is an adenosine nucleotide analogue. During viral RNA synthesis, it incorporates into the nascent RNA and causes premature termination, thus interrupting viral RNA production. There are currently 6 ongoing clinical studies, some of which are large-scale phase 3 trials; and initial results are encouraging. However, as an experimental drug, Remdesivir is not expected to be available in large amounts very soon.
Chloroquine and its derivative hydroxychloroquine had recently made headlines thanks to early reports from China and France about its effectiveness in treating severely ill COVID-19 patients. Having been used to treat malaria and some autoimmune diseases, these drugs are readily available. In laboratory studies, the drugs have been shown to block entry of the virus by interfering with host cell receptor. In addition, they also inhibit virus/host cell fusion, preventing the release of viral nucleocapsid. However, more recent human studies suggest that these drugs may produce serious side effects that can be fatal. Specifically, they may cause QT interval prolongation, an abnormal heart rhythm that can quickly develop into lethal rhythms of ventricular tachycardia and fibrillation. The FDA now recommends against taking chloroquine or hydroxychloroquine for COVID-19 infections unless they are prescribed in hospitals under close supervision, or as part of a clinical trial.

Understanding the Virus that Causes COVID-19, with Animation

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Coronaviruses are a large family of enveloped, RNA viruses. There are 4 groups of coronaviruses: alpha and beta, originated from bats and rodents; and gamma and delta, originated from avian species. Coronaviruses are responsible for a wide range of diseases in many animals, including livestock and pets. In humans, they were thought to cause mild, self-limiting respiratory infections until 2002, when a beta-coronavirus crossed species barriers from bats to a mammalian host, before jumping to humans, causing the Severe Acute Respiratory Syndrome, SARS, epidemic. More recently, another beta-coronavirus is responsible for the serious Middle East Respiratory Syndrome, MERS, started in 2012. The novel coronavirus responsible for the Coronavirus Disease 2019 pandemic, COVID-19, is also a beta-coronavirus. The genome of the virus is fully sequenced and appears to be most similar to a strain in bats, suggesting that it also originated from bats. The virus is also very similar to the SARS-coronavirus and is therefore named SARS-coronavirus 2, SARS-CoV 2. At the moment, it’s not yet clear if the virus jumped directly from bats to humans, or if there is a mammalian intermediate host.

Coronavirus genome is a large, single-stranded, positive-sense RNA molecule that contains all information necessary for the making of viral components. The RNA is coated with structural proteins, forming a complex known as nucleocapsid. The nucleocapsid is enclosed in an envelope, which is basically a LIPID membrane with embedded proteins. From the envelope, club-like spikes emanate, giving the appearance of a crown. This is where the “corona” name came from.

The integrity of the envelope is essential for viral infection, and is the Achilles’ heel of the virus, because the lipid membrane can easily be destroyed by lipid solvents such as detergents, alcohol and some disinfectants. In fact, enveloped viruses are the easiest to inactivate when they are outside a host.

In order to infect a host cell, the spikes of the virus must BIND to a molecule on the cell surface, called a receptor. The specificity of this binding explains why viruses are usually species specific – they have receptors in certain species, and not others. Host jumping is usually triggered by mutations in spike proteins which change them in a way that they now can bind to a receptor in a new species.

The novel coronavirus appears to use the same receptor as SARS-coronavirus for entry to human cells, and that receptor is the angiotensin-converting enzyme 2, ACE2. Infection usually starts with cells of the respiratory mucosa, then spreads to epithelial cells of alveoli in the lungs.

Receptor binding is followed by fusion of the viral membrane with host cell membrane, and the release of nucleocapsid into the cell. The virus then uses the host machinery to replicate, producing viral RNAs and proteins. These are then assembled into new viral particles, called virions, by budding into intracellular membranes. The new virions are released and the host cell dies.

Uncontrolled growth of the virus destroys respiratory tissues, producing symptoms. Infection triggers the body’s inflammatory response, which brings immune cells to the site to fight the virus. While inflammation is an important defense mechanism, it may become excessive and cause damage to the body’s own tissues, contributing to the severity of the disease. In an otherwise healthy person, there is a good chance that the virus is eventually eliminated and the patient recovers, although some may require supportive treatments. On the other hand, people with weakened immune system or underlying chronic diseases may progress to severe pneumonia or acute respiratory distress syndrome, which can be fatal.

Medical Information Illustrated

Medical and health topics fully illustrated with pictures and videos for easy understanding.