Coronavirus Facts and Myth Buster

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Dr KK Aggarwal Research Fund

With inputs from Dr Monica Vasudev

Small risk of bleeding and clotting disorders after AstraZeneca vaccine

There is a small increased risk of immune thrombocytopenic purpura (ITP) and other bleeding and vascular events associated with the Oxford/AstraZeneca vaccine, as per a nationwide analysis of over 2.5 million Scottish adults published in the journal Nature Medicine. These participants had received a first dose of the Oxford/AstraZeneca or Pfizer/BioNTech vaccine between December 2020 and April 2021.

  • Oxford/AstraZeneca was associated with a slightly increased risk of ITP up to 27 days after vaccination.
  • The estimated frequency was 1.13 cases per 100,000 first-dose vaccinations.
  • Those at greatest risk of ITP tended to be older (median age, ≥69 years old) and had at least one underlying chronic health problem, such as coronary heart disease, diabetes, or chronic kidney disease.
  • A very small increased risk of other arterial blood clot and bleeding events associated with Oxford/AstraZeneca up to 27 days after vaccination was also seen. However, there were insufficient data to conclude that there was an association between Oxford/AstraZeneca and cerebral venous sinus thrombosis.

However, the research suggests that the risks are comparable with those seen with other vaccines, including vaccines against hepatitis B, measles, mumps and rubella and influenza.

There was no evidence of an increased risk of the adverse events studied associated with the Pfizer/BioNTech vaccine.

(Source: Dawn OShea. Scottish study estimates risk of bleeding and clotting disorders after AstraZeneca vaccine - Medscape - Jun 09, 2021)

Patients with migraine have higher Covid incidence

A cross-sectional study from the United States has reported higher incidence of Covid-19 as well as heightened COVID symptoms in people who suffer migraines. The study was presented at the American Headache Society virtual meeting.

The study included 66,585 participants, aged 18 to 65 years, in the National Health and Wellness Survey (NHWS); 77% of the respondents were female. Of these, 7,759 people had a migraine diagnosis, while 58,827 did not have migraine. Overall, 3.82% of migraine patients self-reported having COVID-19 and 1.32% said they had tested positive for COVID. In contrast, 2.42% of the group without migraine self-reported having COVID and 0.82% of that group said they had tested positive (all P<0.001). Among those with Covid-19, those who had migraine reported more and higher percentages of COVID symptoms. They also were less likely to use healthcare resources if they tested positive for COVID.

Robert Shapiro, MD, PhD, of the University of Vermont in Burlington said, “Headache is a prevalent symptom of COVID-19, of long COVID, and of post-vaccination for COVID-19. Among COVID-19 inpatients, headache is associated with a positive prognosis. IL-6 levels are lower across the disease course. Headache is associated with 1 week shorter disease course overall. And if someone is admitted with COVID with a symptom of headache, it confers positive relative risk of survival of 2.2.”

(Source: Medpage Today, June 9, 2021)

CVST risk still higher with COVID-19 than with AZ/ J&J vaccination

Rates of cerebral venous sinus thrombosis (CVST) are much higher among patients with Covid-19 compared to persons who have been vaccinated with either the AstraZeneca or the Johnson & Johnson (J&J) vaccine, suggests a study published in the Journal of the American College of Cardiology on June 8.

The rate of CVST associated with the two vaccines was estimated based on the publicly reported data, which was compared to the rate observed among patients hospitalized with Covid-19 and in comparison with the estimated incidence rates among the US population before the pandemic. Data from the United Kingdom Medicines and Healthcare products regulatory agency and the US Centers CDC was used to report the number of events per vaccinated people with the AstraZeneca and Johnson & Johnson vaccines, respectively.

The SVIN COVID-19 multinational study of cerebrovascular events was used to find CVST rates among patients hospitalized with COVID-19. Latest available data from the Nationwide Inpatient Sample database from March and April 2018 were used to report the weighted monthly incidence of CVST before the pandemic.

  • Results showed that as of April 14, 2021, there were 77 CVST cases among 21,200,000 AstraZeneca vaccine recipients reported by the UK Medicines and Healthcare Products Regulatory Agency (3.6 per million; 99% CI, 2.7 – 4.8 per million).
  • As of April 13, 2021, the Centers for Disease Control and Prevention reported six cases of CVST among 6.85 million vaccinated people (0.9 per million; 99% CI, 0.2 – 2.3 per million).
  • In the SVIN COVID-19 registry, 3 of 14,483 patients hospitalized with COVID-19 had CVST (207.1 per million; 99% CI, 23.3 – 757.7 per million).
  • In the Nationwide Inpatient Sample, the weighted average rate of CVST in the US population for March and April 2018 was 2.4 per million (99% CI, 2.1 – 2.6 per million).

The authors conclude: “CVST is rare in the general population and after adenovirus-based SARS-CoV-2 vaccination, but appears to be several-fold more common in hospitalized patients with COVID-19.

Additional research is required to fully elucidate the event rates, to understand the risk factors for vaccine-associated CVST and to identify strategies to prevent it. In the meantime, transparent realistic communication of the risk estimates will be helpful for shared decision making between patients and clinicians.”

(Source: CVST risk still higher with COVID-19 than with AZ, J&J vaccination - Medscape - Jun 10, 2021)

CMAAO Coronavirus Facts and Myth Buster: COVID Surge

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1052: Update on COVID-19: IMA-CMAAO Webinar on “Understanding Coronavirus differently”

15th August, 2020; 4-4.30pm

Participants: Dr KK Aggarwal, President CMAAO, Dr RV Asokan, Hony Secretary General IMA,Dr Ramesh K Datta, Hony Finance Secretary IMA, Dr S Sharma

Faculty: Dr KK Aggarwal, Padma Shri Awardee, President, CMAAO & HCFI

Key points from the discussion

The new coronavirus behaves in six different ways: Viral, bacterial, HIV-like, it causes immunoinflammation, thromboinflammation and cytokine storm.
This virus causes immune (antigen) triggered inflammation wherever ACE2 receptors are present. If there is pre-existing inflammation, it will flare up.
This is a disease of the inflammation of the digestive and metabolic fires of the body.
There are two types of fire or agni in the body: microbiome fire and my agni fire. The balance or imbalance between the two causes health and disease. This virus triggers and increases agni in the body, leading to disruption of the body’s thermostat, resulting in low grade fever.
If baseline CRP is less than 1, then no impact; if 1-3, then exacerbation of fire, and if more than 3, then there is high hyperinflammation leading to vasculitis, thrombus formation, neoangiogenesis and hypoxia.
The route of entry is GI or respiratory tract. The virus may be present in GI system much before it is seen in the respiratory system and even if not seen in the respiratory tract.
Skin biopsy may also be positive for the virus (Lancet).
If fragments of the antigen persist, the person may be a carrier; they may also cause recurrence of symptoms, reactivation of illness and trigger inflammation.
There are six antigens in COVID-19 virus: E, S, N, ORF 1a, ORF 1b and RDRP antigen. The RT PCR test assesses the antigens and not the virus.
E antigen is a must; it is common for all coronaviruses. If negative, no corona.
We do not know yet which antigen persists for more than 9 days. We must find out which of these antigens is infectious.
When we say RT PCR is positive, it is important to know which antigen is positive.
True Nat tests RDRP; Singapore, at airports, is testing N, ORF and S.
If we find out which part of the virus (antigen) is causing which inflammation, this could be a game changer.
In patients with insulin resistance, where there is already low grade inflammation, the trigger is faster and more significant.

Dr KK Aggarwal

President CMAAO, HCFI and Past National President IMA

CMAAO Coronavirus Facts and Myth Buster: RTPCR Memory T Cells

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With inputs from Dr Monica Vasudev

1046: A spurt of new studies has shown that a large proportion of the population — at some places, around 20-50% of people — might carry T cells that identify the new coronavirus despite having never encountered it before. Although it’s too early to ascertain how helpful they might be, but even a slight influence on immune response could make the disease milder.

While the new coronavirus was unknown until 8 months back, yet to some human immune cells, it was already something familiar.

This could be a case of family resemblance. For the immune system, pathogens with common roots can look alike, such that when a similar pathogen comes to call, the body may already have a clue of its intentions.

The presence of T cells has fascinated the experts, who state that it is too early to be able to tell if the cells will play a helpful, harmful or negligible role against the new coronavirus.

However, if these T cells exert even a modest influence on the body’s immune response, the disease might become milder. This could, in part, explain why some people become very sick while others don’t. (New York Times Excerpt)

SARS-CoV-2-specific T cell immunity in COVID-19, SARS and uninfected controls

Memory T cells that are induced by previous pathogens can build the susceptibility to, and clinical severity of, subsequent infections. There is limited information about the presence of pre-existing memory T cells in humans with the potential to recognize SARS-CoV-2.

In a recent paper published in Nature, researchers assessed T cell responses to structural (nucleocapsid protein, NP) and non-structural (NSP-7 and NSP13 of ORF1) regions of SARS-CoV-2 in 36 COVID-19 convalescents. Investigators noted the presence of CD4 and CD8 T cells recognizing multiple regions of the NP protein in all of them. Twenty three SARS-recovered patients were still found possess long-lasting memory T cells that were reactive to SARS-NP nearly 17 years after the 2003 outbreak, showing strong cross-reactivity to SARS-CoV-2 NP.

SARS-CoV-2 specific T cells were also identified in individuals with no history of SARS, COVID-19 or contact with SARS/COVID-19 patients (n=37).

SARS-CoV-2 T cells detected in uninfected donors had a different pattern of immunodominance, frequently targeting the ORF-1-coded proteins NSP7 and 13 as well as the NP structural protein.

Epitope characterization of NSP7-specific T cells exhibited recognition of protein fragments with low homology to ‘common cold’ human coronaviruses but it was conserved amongst animal beta-coranaviruses.

Therefore, infection with beta-coronaviruses tends to induce multispecific and long-lasting T cell immunity to the structural protein NP.

Understanding how pre-existing NP- and ORF-1-specific T cells present in the general population affect the vulnerability and pathogenesis of SARS-CoV-2 infection is important for the management of the COVID-19 pandemic.

[Bert NL, et al. Nature (2020)]

Dr KK Aggarwal

President CMAAO, HCFI and Past National President IMA

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