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Tuesday, 16 June 2020

What we still don’t know about deadly coronavirus

Kibra Covid-19
Months into the pandemic, questions abound on a number of issues. Scientists are still trying to figure out Sars-Cov-2, the Covid-19-causing virus, and there are many studies trying to explain some of these mysteries. The answers to these questions could unlock the much-needed treatment for the disease.

1. The numbers riddle
As of yesterday, 3,727 people had tested positive for Covid-19 in Kenya, but many scientists fear there could be hundreds, or even thousands, of people who have been infected. Scientists believe the actual number of cases is higher, they just do not know by how many because there are still people who have not been tested.
Earlier, the Ministry of Health had estimated that the government’s modelling had projected that 5,000 people in the country  would have the virus by April. This month, the numbers are not only far from the estimated, but also the University of Nairobi has projected another ghastly statistic: by February 2021, about two million Kenyans would be sick of the virus, but be asymptomatic. 
In a research paper published in preprint, Peter Macharia, a researcher from Kenya Medical Research Institute (Kemri) Wellcome Trust programme, listed 24 factors that would make some counties more vulnerable than others. Featured in the list were issues such as the immunity of a population judging by their age or other diseases that they suffer from such as HIV, and the ability to access healthcare. Further additions were contained in a study done by the Institute of Economic Affairs (IEA), which included other factors such as free movement made easy by robust transport systems.  
With this in mind, Nairobi and Mombasa are not the only towns in Kenya that could have many people with the virus.  Health Cabinet Secretary Mutahi Kagwe has said out of all the positive cases, about nine in 10 (89 per cent) are local transmissions, with Nairobi having nearly half (45 per cent) of the cases, followed closely by Mombasa (30 per cent). 
IEA’s analysis of the vulnerability of counties to Covid-19 revealed that Kenya’s busiest counties - Nairobi, Mombasa, Nakuru and Kiambu - are at the highest risk. 
Kwame Owino, Chief Executive Officer of IEA, said the risks include how busy the towns are, and movement in and out of the town. Their closeness to Nairobi also made them extremely vulnerable. The populations of Nakuru, Kiambu and Machakos are above 1.4 million.
It seems impossible to imagine that any contact-tracing programme, an old ‘boots-on-the-ground’ tactic in disease control, will be able to keep up with that:  even when the more than 70,000 community health volunteers in Kenya are deployed, there will not be enough people to follow each Kenyan.

2. How youth fits into this puzzle
The low number of cases reported in Africa continues to puzzle scientists. Matters get complicated when Kenya’s youthful population comes into question. Kariuki Njenga, a Kenya based professor of infectious diseases from Washington State University, published a paper in the American Journal of Tropical Medicine and Hygiene attributing the low Covid-19 mortality in Africa to its youthful population.
Africa’s more youthful population, with a median age of less than 20 years, when compared with those in Europe and the US, whose median age is greater than 38 years, may have contributed to the low numbers of severe Covid-19 cases and deaths. However, this population has also been blamed for the spread of the disease. Health Director-General Patrick Amoth termed the young people “super spreaders”.  Those between 15 and 35 years old are often asymptomatic, but are able to move around spreading the virus to those with compromised immunities and most likely to fall sick. 
There are also many crucial unresolved questions about children and Covid-19. These answers are important for people and their families and the society at large as the country explores the possibilities of reopening schools. One puzzle is what role children play in spreading the virus. They seem less likely to become seriously ill than adults, making up less than two per cent of Kenya’s coronavirus cases. There are different theories about whether that is because children are less likely to become infected to begin with, or whether the virus infects them just as easily, but mostly causes few or no symptoms.
Either way, a growing body of evidence suggests that infected children can transmit the virus, possibly as easily as adults. And one recent study suggests that when children attend school, they come in contact with three times as many people as average adults do, providing more opportunities for children to become infected and infect others.
Although far fewer children than adults have experienced severe symptoms, some children have become devastatingly ill. Reports from hospitals suggest that the children most vulnerable to the respiratory failure adults develop are those who already have a serious medical condition. Some studies also suggest that infants and preschoolers may be more vulnerable than older children.

3. Who was first may always be a mystery
The notion of a single patient zero is both theatrical and real: In any new epidemic, some unlucky soul seeds the first infection, several links of which are fated to seed chains of their own and spark a viral Big Bang.
By analysing the genetic material of people who test positive, scientists can trace the lineage of each virus back to a common ancestor and often to an individual carrier. The first confirmed coronavirus case in Kenya was a Kenyan woman who travelled back to Nairobi from the US through London, UK, on March 5. 
While the government is not evangelical about tracking where the infections sprang from, scientists from Kemri have found genetic signatures on the viruses studied so far linking them to China, South Africa and Europe, probably brought in by some of hundreds of the arrivals in Nairobi prior to the lockdowns.
Prof Thumbi Ndung’u, a Kenyan scientist in South Africa, told HealthyNation it was likely that there were multiple introductions that spread widely in Nairobi and Mombasa. So, patients zero, plural. This is because the first infected arrivals in a community are not necessarily the ones who light the fuse. The jury is still out on whether the March 13 case was the first one, and it is possible that there were people who fell ill earlier than this. 
The level of detective work required to find the actual patient zero might be steeper than it appears. At least one genetic scientist has argued that the virus could have first infected humans — likely from a pangolin — well before last fall in a form that did not cause sickness. It then evolved its pathogenic features over time while circulating. If that is the case, the question “Who came first?” may go without a conclusive answer for some time, perhaps for good.

4. You are immune, but will it last?
Are people infected with the coronavirus protected from further infection? And, if yes, for how long? The answers to these questions have broad implications for reopening the economy and allowing the public to live with less fear of infection in the short term — and for the effectiveness of vaccines in the long term. Scientists have made steady, if incremental, progress in getting to the answers. 
Prof Ndung’u explained that when the body encounters any virus, it typically makes antibodies, some of which are powerful enough to neutralise the pathogen and prevent reinfection. It also produces large numbers of immune cells that can kill the virus.
Most tests that look for antibodies to the coronavirus have been flawed. But, at least one team with a reliable test reported that most people, including those who were only mildly ill, make powerful antibodies. Data on immune cells has been slower to emerge, but a few studies suggest a robust response from immune cells as well. 
Prof Kariuki Njenga wrote that there could be some immunity that may have been conferred to Kenyans from the exposure from similar viruses including the common cold, or the Middle East Respiratory Syndrome. What remains unknown is how long this immunity will last.
There have been some reports of reinfection, but scientists have said that they are a result either of faulty testing, or of viral remnants that circulate long after the active infection has ended.
According to World Health Organization, most studies on antibody response to Covid-19 infection show that people who have recovered from it have antibodies to the virus. However, some of these people have very low levels of neutralising antibodies in their blood, suggesting that cellular immunity may also be critical for recovery. “As of April 24, no study had evaluated whether the presence of antibodies to Sars-Cov-2 confers immunity to subsequent infection by this virus in humans,” adds WHO.

5. Figuring out a receptor’s role
Covid-19 is a mercurial disease. While some people experience only mild, fleeting symptoms, others are knocked over with a severe flulike illness that can last several weeks. A minority of patients develop life-threatening complications, some die.
Why do some people sail through the illness, and others develop the severe inflammation and lung damage that are hallmarks of the disease? It is one of the great mysteries of Covid-19.
Experts say the patient’s immune response to the viral infection determines the severity of the illness. If the immune system goes into overdrive, it can trigger a cascade of harmful effects, injuring the lungs and other organs.
Immune function declines with age, and elderly people with Covid-19 are among the most vulnerable to poor outcomes, as are those with chronic health conditions like high blood pressure, diabetes and cardiovascular disease. Obesity, which is a public health concern in Kenya, also appears to exacerbate the illness.
Other susceptibilities are harder to explain. Men are also at greater risk for critical illness and death. Kenya has continuously reported more cases of men being infected than women. For instance, of the 137 cases reported by the Health ministry on Sunday, 102 were men. This sex disparity may be explained by women’s more robust immune systems, scientists say. Others have explained it as a difference brought about by lifestyle choices: In some countries there are more men smokers than women. Smoking affects the level of diseases such as cancer, lowering one’s immunity.
Generally speaking, patients get sicker faster if they are exposed to a large dose of the virus when they are first infected, said Dr William Schaffner, an infectious disease specialist at Vanderbilt University.
Much scientific inquiry has focused on the role of a receptor called angiotensin-converting enzyme 2, or Ace2, which is the entry way for coronaviruses into the cells. The receptor is found on the outer surfaces of cells in the lungs, blood vessels, intestines and other organs, as well as in the back of the throat and high up in the nasal passage.
When the pandemic started, there was a concern that people taking blood pressure medications like Ace inhibitors could be at greater risk from the coronavirus, but so far studies have not found that to be the case, and doctors are urging patients to continue their medication.
Though the Sars-Cov-2 virus attaches to the receptor in order to penetrate cells, Ace2 also helps regulate blood pressure and inflammation. Some scientists have suggested that children may be less susceptible to infection with Covid-19 because they have fewer of these receptors. Ace2 is also regulated differently in men and women, according to scientists who study sex differences in medicine, and men tend to develop hypertension, or high blood pressure, at younger ages than women. But, much is still unknown.
“Ace2 can play two very critical roles, getting the virus into the cell, but also modulating some of the damage that takes place in the blood vessels and the lungs,” said Dr Ankit Patel, a nephrologist at Brigham and Women’s Hospital in Boston in the US. “So it’s a double-edged sword in a sense, and that’s made the whole story all the more complicated.”

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