Tag Archives: SARS-CoV-2

Immune cells from the common cold offer protection against COVID-19, researchers find

If one in 10 cold infections are from coronaviruses, then antibodies produced from these illnesses could surely give a bit more protection against COVID-19, right? A new study has just provided the answer to this question by showing that immunity induced by colds can indeed help fight off the far more dangerous novel coronavirus.

Image credits: Engin Akyurt.

A study from Imperial College London that studied people exposed to SARS-CoV-2 or COVID-19 found that only half of the participants were infected, while the others tested negative. Before this, researchers took blood samples from all volunteers within days of exposure to determine the levels of an immune cell known as a T cell – cells programmed by previous infections to attack specific invaders.

Results show that participants who didn’t test positive had significantly higher levels of these cells; in other words, those who evaded infection had higher levels of T cells that attack the Covid virus internally to provide immunity — T cells that may have come from previous coronavirus infections (not SARS-CoV-2). These findings, published in the journal Nature Communications, may pave the way for a new type of vaccine to prevent infection from emerging variants, including Omicron.

Dr. Rhia Kundu, the first author of the paper from Imperial’s National Heart & Lung Institute, says: “Being exposed to the SARS-CoV-2 virus doesn’t always result in infection, and we’ve been keen to understand why. We found that high levels of pre-existing T cells, created by the body when infected with other human coronaviruses like the common cold, can protect against COVID-19 infection.” Despite this promising data, she warns: “While this is an important discovery, it is only one form of protection, and I would stress that no one should rely on this alone. Instead, the best way to protect yourself against COVID-19 is to be fully vaccinated, including getting your booster dose.”

The common cold’s role in protecting you against Covid

The study followed 52 unvaccinated people living with someone who had a laboratory-confirmed case of COVID-19. Participants were tested seven days after being exposed to see if they had caught the disease from their housemates and to analyze their levels of pre-existing T cells. Tests indicated that the 26 people who tested negative for COVID-19 had significantly higher common cold T cells levels than the remainder of the people who tested positive. Remarkably, these cells targeted internal proteins within the SARS-CoV-2 virus, rather than the spike protein on its surface, providing ‘cross-reactive’ immunity between a cold and COVID-19.

Professor Ajit Lalvani, senior author of the study and Director of the NIHR Respiratory Infections Health Protection Research Unit at Imperial, explained:

“Our study provides the clearest evidence to date that T cells induced by common cold coronaviruses play a protective role against SARS-CoV-2 infection. These T cells provide protection by attacking proteins within the virus, rather than the spike protein on its surface.”

However, experts not involved in the study caution against presuming anyone who has previously had a cold caused by a coronavirus will not catch the novel coronavirus. They add that although the study provides valuable data regarding how the immune system fights this virus, it’s unlikely this type of illness has never infected any of the 150,000 people who’ve died of SARS-CoV-2 in the UK to date.

Other studies uncovering a similar link have also warned cross-reactive protection gained from colds only lasts a short period.

The road to longer-lasting vaccines

Current SARS-CoV-2 vaccines work by recognizing the spike protein on the virus’s outer shell: this, in turn, causes an immune reaction that stops it from attaching to cells and infecting them. However, this response wanes over time as the virus continues to mutate. Luckily, the jabs also trigger T cell immunity which lasts much longer, preventing the infection from worsening or hospitalization and death. But this immunity is also based on blocking the spike protein – therefore, it would be advantageous to have a vaccine that could attack other parts of the COVID virus.

Professor Lalvani surmises, “The spike protein is under intense immune pressure from vaccine-induced antibodies which drives the evolution of vaccine escape mutants. In contrast, the internal proteins targeted by the protective T cells we identified mutate much less. Consequently, they are highly conserved between the SARS-CoV-2 variants, including Omicron.” He ends, “New vaccines that include these conserved, internal proteins would therefore induce broadly protective T cell responses that should protect against current and future SARS-CoV-2 variants.”

COVID-19 antibodies last as long as 8 months

Illustration of antibodies (red and blue) responding to an infection with the new coronavirus SARS-CoV-2 (purple). The virus emerged in Wuhan, China, in December 2019, and causes a mild respiratory illness (COVID-19) that can develop into pneumonia and be fatal in some cases.

Our current understanding of SARS-CoV-2 immunity is mainly based on previous experiences with SARS-CoV (2003) and recent studies in patients infected with and recovered from SARS-CoV-2 (2020). 

Similar to the SARS-CoV infection, the main antibody targets in SARS-CoV-2 are the spike and nucleocapsid proteins (NCP) — and this is where the vaccines also strike. However, it’s not clear if lasting immunity against the novel coronavirus can be achieved because serum antibodies seem to decline. Since this pandemic is still relatively new, we haven’t had much time to explore just how long antibodies and immunity lasts — but new results are coming in.

Two new studies published recently demonstrate that COVID-19 antibodies last as long as 8 months, or potentially even more, giving some good news for a mass vaccination campaign.

A study published in Science Immunology followed a small cohort of Australians from day 4 to day 242 after infection. All patients demonstrated the presence of memory B cells — immune cells that “remember” viral proteins and can trigger rapid production of antibodies when re-exposed to the virus — as long as 8 months after the initial infection.

Researchers took blood samples from 25 confirmed COVID-19 patients with a range of disease severities and 36 healthy control patients from March to September, evaluating each patient’s antibody status and levels of virus-specific immune cells. The study showed that by day 6 post-infection, all patients showed immunoglobulin G (IgG) antibodies for the viral receptor-binding domain (a protein on the viral surface that binds to cell receptors, allowing entry and infection) and the nucleocapsid protein. The immunoglobulin G levels began declining 20 days after symptom onset. However, memory B cell levels continued to rise up to 150 days post-infection and remained detectable 240 days post-symptom onset, suggesting that patient immune systems were primed to respond to reinfection.

According to the authors, cellular immunity could explain why there are few documented cases of reinfection with SARS-CoV-2 and why immunity can last longer than the antibody levels would suggest it.

Another study investigated antibody responses in 58 confirmed COVID-19 patients in South Korea 8 months after asymptomatic or mild SARS-CoV-2 infection.

The team used 4 commercially-available immunoassays:

Except for the anti-N IgG ELISA, all of these immunoassays have been granted Emergency Use Authorization by the US Food and Drug Administration.

For 3 of 4 immunoassays used, seropositivity rates were high (69% to 91.4%; < 0.01). These results, published in Emerging Infectious Diseases, are contradictory to both the first study’s antibody data and previous research that showed antibodies waning after 20 days, but the authors suggest that variations in immunoassay test characteristics and manufacturing may be responsible for the difference.

Increasingly, the scientific evidence seems to suggest

Can aspirin reduce the risk of death in hospitalized COVID-19 patients?

Researchers at the University of Maryland School of Medicine showed COVID-19 patients who were taking a daily low-dose aspirin for cardiovascular disease had a significantly lower risk of complications and death compared to those who were not taking aspirin.

The researchers looked through the medical records of 412 COVID-19 patients, age 55 on average, who were hospitalized over the past few months due to complications of SARS-CoV-2 infection. About a quarter of the patients were taking a daily low-dose aspirin (usually 81 milligrams) before they were admitted or right after admission to manage their cardiovascular disease.

The researchers found aspirin use was associated with a 44 percent reduction in the risk of being put on a mechanical ventilator, a 43 percent decrease in the risk of ICU admission, and — most important of all — a 47 percent decrease in the risk of dying in the hospital compared to those who were not taking aspirin. The patients in the aspirin group did not experience a significant increase in adverse events such as major bleeding while hospitalized. The study definitely showed an association or correlation but remember correlation does not mean causation.

Nevertheless, this is promising because if this finding is confirmed (through clinical trials with larger sample size), it would make aspirin the first widely available, over-the-counter medication to reduce mortality in COVID-19 patients. Aspirin is a very potent antiplatelet agent. As soon as aspirin interacts with a platelet, that platelet becomes inactivated and can no longer create clots.

British Heart Foundation | How does aspirin work?

In July a study published in the Journal of the American College of Cardiology reviewed the effect of anticoagulant drugs on outcomes among hospitalized Covid-19 patients. Like the recent aspirin study, the investigators found that anticoagulants significantly reduced the risk of death among certain groups of people with Covid-19. Although these studies are encouraging, we need to wait for further studies to be done. Aspirin came into being in the late 1890s in the form of acetylsalicylic acid when chemist Felix Hoffmann at Bayer in Germany used it for his father’s rheumatism but salicin, which comes from the bark of the willow plant has been widely used hundreds of years before that.

Now, aspirin Is not only used to reduce pain, fever, or inflammation but is also the cornerstone of therapy to prevent a heart attack or a stroke since 1970s but the drug is not without risks. The greatest risk associated with aspirin is gastrointestinal bleeding so people who have a history of peptic ulcers or bleeding from the stomach should not take it.

The good news is the United Kingdom’s Recovery Trial, a large randomized controlled clinical study of potential COVID-19 treatments, will investigate aspirin as a possible therapy. Why aspirin? Patients with COVID-19 are at higher risk of blood clots forming in their blood vessels. Platelets, small cell fragments in the blood that stop bleeding, seem to be hyperreactive in COVID-19 and may be involved in the clotting complications.

Aspirin is already widely used to prevent blood clots in many other conditions but enrolling patients in a randomized clinical trial is the best way to assess whether there are clear benefits for patients with COVID-19 and whether those benefits outweigh any potential side-effects such as the risk of bleeding. At least 2,000 patients are expected to get 150mg of aspirin daily along with the usual regimen. Hopefully, in a few months, we’ll know whether aspirin is indeed good for patients with COVID-19.

The Recovery trial was the first to show that dexamethasone, a steroid that is also cheap and widely available, could save the lives of people severely ill with Covid-19. It also showed that the anti-malarial drug hydroxychloroquine provided no benefit in treating COVID-19 patients.

Symptomatic and asymptomatic COVID-19 patients shed virus similarly

We are learning more about how COVID-19 affects people every day, and this new find confirms what we’ve been fearing: asymptomatic people can pass the virus with the same ease.

 We know that SARS-CoV-2, the virus causing COVID-19, is transmitted through direct contact with respiratory droplets of an infected person (generated through coughing and sneezing). Individuals can also be infected from and touching surfaces contaminated with the virus and touching their face (e.g., eyes, nose, mouth). The COVID-19 virus may survive on surfaces for several hours, but simple disinfectants can kill it.

Available evidence from contact tracing reported by countries suggests that asymptomatically infected individuals are much less likely to transmit the virus than those who develop symptoms. However, researchers from South Korea reported in JAMA Internal Medicine that patients with confirmed asymptomatic COVID-19 infections shed virus at similar levels to those who are experiencing symptoms. “Viral shedding” refers to the release of the virus from an infected host. The investigators concluded that “isolation of infected persons should be performed regardless of symptoms.”

Their cohort study involved 303 patients who were isolated at a community treatment center in Cheonan in March. Healthcare workers carefully tracked patients’ symptoms during isolation. Among the group, 193 (63.7%) had symptoms at the start of isolation and 21 (19.1%) of the asymptomatic patients went on the develop symptoms. Healthcare workers also conducted reverse transcription polymerase chain reaction (RT-PCR) tests on lower and upper respiratory tract samples on multiple days at doctor discretion. Cycle threshold values for SARS-CoV-2 were similar for both asymptomatic and symptomatic patients. Viral shedding lasted about 17 days in asymptomatic patients and 19.5 days for symptomatic and pre-symptomatic patients.

Why are some people asymptomatic while others are not? SARS-CoV-2 uses the angiotensin-converting enzyme 2 (ACE2) as a cell receptor to invade human cells. Using the spike-like protein on its surface, the SARS-CoV-2 virus binds to ACE2 – like a key being inserted into a lock – prior to entry and infection of cells. Hence, ACE2 acts as a cellular doorway.

The ACE2 receptors appear to be more prevalent in older people and those who are obese than in younger and healthier people. That may partly explain why so many young people have not been as badly affected by the virus as those older than 60. Previous exposure to other coronaviruses, which can give people “T-cell immunity” to similar viruses, receiving a lower viral load of COVID-19 and other lucky genetic variations may also contribute to why some people having less severe or not symptoms to infection.

The coronavirus epidemic could be fueling higher rates of delirium, brain inflammation, stroke, and nerve damage

A new study from the University College London (UCL) worryingly reports that COVID-19 can lead to complications such as delirium, brain inflammation, stroke, or nerve damage.

A 3D-printed human brain.
Image credits Flickr / NIH Image Gallery.

The study identified one rare but sometimes fatal inflammatory condition known as acute disseminated encephalomyelitis (ADEM) which has been increasing in prevalence during the epidemic. While ADEM itself is quite rare and usually seen in children, the team found a high prevalence of this condition among COVID-19 patients suffering from neurological symptoms.

Not good for the brain

“We should be vigilant and look out for these complications in people who have had COVID-19. Whether we will see an epidemic on a large scale of brain damage linked to the pandemic—perhaps similar to the encephalitis lethargica outbreak in the 1920s and 1930s after the 1918 influenza pandemic—remains to be seen” says joint senior author Dr. Michael Zandi from the UCL Queen Square Institute of Neurology.

The team analyzed the cases of 43 people (aged 16-85) being treated at the National Hospital for Neurology and Neurosurgery, UCLH, who were confirmed with COVID-19. ADEM, they explain, has a surprisingly-high prevalence among this group.

Some patients didn’t experience any severe respiratory symptoms, with their neurological disturbances being the first main indications of COVID-19. The team identified 10 cases of transient encephalopathies (temporary brain dysfunction) with delirium, 12 cases of brain inflammation, 8 cases of stroke, and 8 patients with nerve damage, mainly Guillain-Barré syndrome.

Some patients in the study did not experience severe respiratory symptoms, and the neurological disorder was the first and main presentation of COVID-19.

The authors describe this as a “higher than expected number of people with neurological conditions” and explain that these did not always correlate with the intensity of their respiratory symptoms.

Out of the 12 cases of brain inflammation, 9 were diagnosed with ADEM. Typically, the team says one adult patient with ADEM will come in every month, but this has increased in frequency to at least one per week since the start of the pandemic.

How it does this is still unclear

The coronavirus attacks the respiratory system first and foremost. This is a chest tomography of a 38 years old male patient. The white “grid-like lobules” represent areas where the virus is attacking tissues.
Image via Wikimedia.

SARS-CoV-2 was not detected in samples of cerebrospinal fluid from any of the patients, however. This suggests that the virus isn’t directly responsible for the neurological symptoms (i.e. it doesn’t attack brain tissue itself). However, that also means we’re not sure, for now, exactly why these symptoms appear — more research is needed to find out. Preliminary data suggests that at least some patients are experiencing these symptoms due to their own immune response to the disease.

“Given that the disease has only been around for a matter of months, we might not yet know what long-term damage Covid-19 can cause,” says joint-first author Dr. Ross Paterson from the UCL Queen Square Institute of Neurology.

“Doctors need to be aware of possible neurological effects, as early diagnosis can improve patient outcomes. People recovering from the virus should seek professional health advice if they experience neurological symptoms.”

The findings align well with previous work into the neurological symptoms of SARS-CoV-2. And while the ever-growing list of symptoms this virus seems to cause is definitely worrying, the more we know about what it does the better we can fight those symptoms.

If these neurological effects are indeed caused by our own immune systems, immunosuppressants could be used to eliminate them entirely (along with a host of the virus’ damaging effects). For now, we need to better understand how these neurological symptoms arise, and how to safely combat them — and studies such as this one show us where to start.

The paper “The emerging spectrum of COVID-19 neurology: clinical, radiological and laboratory findings” has been published in the journal Brain.

Researchers document how asymptomatic COVID-19 cases unknowingly spread the coronavirus

study published mid-April reported that people infected with SARS-CoV-2, the coronavirus causing COVID-19, might be most contagious during the period before they have symptoms. Two studies published in late May showed that a high percentage of people with COVID-19 could be without symptoms.

In one study, Australian researchers reported that 104 of 128 people (81 percent) on a cruise ship who tested positive for the novel coronavirus were asymptomatic. In another study, researchers in Wuhan, China reported that 33 of 78 people (42 percent) who tested positive for COVID-19 were without symptoms.

Most recently, a multicenter study published in Travel Medicine and Infectious Disease shows that 60% of asymptomatic (symptom-free) COVID-19 patients in Sichuan province, China, were diagnosed as having pneumonia on their first computed tomography (CT) scan.

The study involved 100 asymptomatic and 411 symptomatic coronavirus patients in hospitals in 21 cities and 47 counties or districts from Jan 25 to Feb 20. The investigators also found that patients without symptoms were younger and came from higher-altitude areas with less resident mobility and more defined epidemiologic history than patients with symptoms but had similar rates of underlying conditions.

Of the 100 well-documented asymptomatic cases, 17 (27.4%) later developed symptoms, two of the older patients developed severe symptoms during hospitalization. No asymptomatic patients died. One patient was believed to have transmitted the virus during the incubation period.

In a May 30 letter to the editor published in Influenza and Other Respiratory Viruses, public health experts describe a likely asymptomatic COVID-19 spread in a household and school after travelers returned to Brunei after attending a religious event in Malaysia from Feb 28 to Mar 2.

Of the more than 4,000 confirmed cases linked to the event, 19 from Brunei tested positive for COVID-19 and infected 52 others. According to the researchers, this is the first report documenting the role of asymptomatic SARS‐CoV‐2 transmission in the propagation of a large superspreading event.

The authors said that their findings support the use of testing and longitudinal surveillance of asymptomatic close contacts, as well as widespread testing at mass gatherings in places with known community spread.

US Centers for Disease Control and Prevention | Your cloth face covering may protect them. Their cloth face covering may protect you.

All these studies strengthen the argument for people to wear masks. After first telling the public there was no need for people to wear a mask unless they were sick or coughing, the US CDC revised their position. Since early April, the agency has recommended that in addition to physical distancing measures, people should wear a face covering if they go to a public place in settings where physical distancing measures are difficult to maintain (e.g., grocery stores and pharmacies) especially in areas of significant community-based transmission. They have posted instructions on how to properly wear a cloth mask.


New study shows sunlight can inactivate SARS-CoV-2

Increasingly, it is being shown that COVID-19 tends to spread faster and easier indoor than outdoor.

Previous studies have demonstrated that SARS-CoV-2, the virus that causes COVID-19, is stable on surfaces for extended periods of time, under indoor conditions.

A research from China showed that coronavirus transmission still takes place despite changing weather conditions in different parts of the country — ranging from cold and dry to warm and humid. A study in Hong Kong using SARS-CoV-2 in a lab solution showed that increasing temperature decreased the amount of viable virus that could be detected. No infectious virus remained after 30 minutes at 56° Celsius and five minutes at 70°C was enough to inactivate the pathogen.

Now, a new study by researchers at the National Biodefense Analysis and Countermeasures Center, a government biodefense research laboratory created by the U.S. Department of Homeland Security, shows that natural sunlight can rapidly inactivate SARS-CoV-2 on surfaces.

The findings, which come with caveats, suggest that the potential for fomite transmission may be significantly reduced in outdoor environments exposed to direct sunlight.

Sunlight vs COVID

To evaluate the influence of simulated sunlight on the persistence of SARS-CoV-2 on surfaces, the researchers exposed concentrated virus suspended in either simulated human saliva or culture media and then dried on stainless steel coupons mounted in a chamber to a light spectrum designed to represent natural sunlight. The coupons were exposed to the simulated sunlight for differing exposures, ranging from 2 to 18 minutes, to allow estimation of the viral inactivation rate. For comparison, the researchers also exposed a series of contaminated coupons in the chamber with no simulated sunlight for 60 minutes.

The results showed that under levels of simulated sunlight representative of midday on the summer solstice at 40°N latitude (the 40th Parallel), 90% of infectious virus is inactivated every 6.8 minutes in simulated saliva dried on a surface and every 14.3 minutes in cultured media dried on a surface. Significant inactivation also occurred under lower simulated light levels but at a slower rate. Inactivation rates were near zero on the coupons not exposed to sunlight.

The inactivation rate of SARS-CoV-2 was approximately two-fold greater in simulated saliva than in culture media. However, the researchers say it is unclear if the viral concentrate in simulated salvia is representative of contaminated saliva from an infected individual. This is good news but do not assume that summer months will be safer.

Sunlight has been in the COVID-19 news cycle for another reason – it is a great natural source of vitamin D, which has several health benefits, including an increased resistance to infectious diseases. When it comes to COVID-19, research is limited but clinical trials have started in Spain and France to see if vitamin D improves outcomes for COVID-19 patients. Both studies are expected to end in July 2020. In the meantime, continue to take appropriate steps to protect yourself and those around you.