Human behavior determines how infectious diseases spread.
- The Ebola outbreak in West Africa between 2014 and 2016 made it even more apparent why anthropologists could help medical authorities consider local cultural and social characteristics in their response to virus outbreaks. That outbreak also provided new perspectives on the origin of social and individual attitudes during epidemics and how to assist grieving families.
How is the role of the anthropologist changing in the study of the spread of infectious diseases?
What role can anthropologists play in a public health crisis like the one we are facing now with Covid-19?
- Every epidemic is unique, but anthropologists can point out the parallels with other sources of epidemics and therefore suggest what made them have their particular shapes and their particular outcomes, to provide us with a basis for understanding what’s going on.
- The second role is to be able to push people outside of the frame of “Now, this is Covid-19,” to be able to understand the underlying factors that helped shape the current situation.
Social and Cultural Factors in Disease
It is not entirely by accident in the United States that right now you have massive protests against police violence that targets particularly African Americans and that Covid-19 is massively differentially killing POC.
- It’s extremely important to ask what are the underlying factors of race, racism and unequal distribution of resources in the United States that are affecting who lives and who dies.
- Otherwise, people tend to rationalize the effects of an epidemic as being dependent upon the cultural or biological characteristics of particular populations as responsible for their own differential rates of infection and death instead of asking what is it about society that renders some people more likely to get infected and more likely to die.
Why do societies tend to think of such events as unprecedented despite having been through similar situations before?
- A crisis tends to make a particular period of time separated off and seemingly unrelated to what goes before it and to what will happen afterwards once we return to normal.
- But if you look at it in deeper anthropological or epidemiological terms, you find that what happens before and what happens next are themselves not normal.
- It is not normal that vastly more African American women die of complications of childbirth, or that infant mortality among African Americans is much greater, and that indigenous people all over the world face the worst health conditions.
- Think of the Navajo Nation, which has the highest percentage of infections per capita in the United States. That’s not unprecedented. That’s precisely a characteristic of little things like access to drinking water.
- but also, as of September 15, the Navaho Nation has brought the infection rate down to zero. How did they do this?
The different rates of infection and death among different racial and social groups is hard to miss. Can this recognition lead to significant changes?
- One of the most familiar results of epidemics is deepening the inequities that caused them.
- The effects of the mitigating measures are not randomly distributed. We need to ask who will be out of work or unemployed for years? Who will have acute food shortages in the future? That’s what’s most crucial for the society, which is also right now experiencing this tremendous movement that has been going on for a long time.
- All of a sudden, the killing of George Floyd made that movement visible and unmistakable, so now that’s beginning to have a transformative effect.
- If the epidemic could potentially have this transformative effect, this would be a very different outcome than the usual one of simply making things worse for the people who have it worst. (what we do after the train stops...How can anthropology contribute to this?
- If these established ways of thinking are part of the problem, you don’t want just to recycle them in an epidemic.
- An epidemic should challenge anthropologists and public health scholars, historians, journalists and all of us to develop new ways of thinking about disease, epidemics, people, and health systems.
Prepare for future social and cultural consequences?
- A report published by the Institute of Medicine in the United States in 2003 under the title of “Unequal Treatment” suggested that African Americans and Latinos—even after taking into account socioeconomic status and health insurance—receive worse medical treatment in the United States. Why?
- Bias: Because thinking of the good patient as normatively white, an African American or Latino walks into a doctor’s office and is seen as not white and therefore as not as rational, not as capable of understanding what the doctor says, not as likely to take the pills or do the exercise, so even a good doctor is more likely to give bad treatment.
- Anthropology can challenge the logics that make these categories seem stable and autonomous
- Categorical subordination leads to stigmatization and further denial of resources
- The 1918–1920 Spanish flu was the last influenza pandemic that really swept the world, and it was effectively lethal to 50 million people. The world population has grown ten-fold since 1918, so that 50 million today would be 500 million.
- The flu from 1918 really was a different virus completely than coronavirus. But these viruses do have in common that the pandemic strains of flu and the coronavirus both came from animals and both are respiratory viruses in humans.
- Flus have a very high mutation rate, a change in the nucleotides that make up the virus’ chromosomes. In that way flu escapes the immune system’s attempts to kill it.
- Influenza viruses are unusual because we can become infected by a similar virus almost every year during our lifetime and occasionally there are worldwide pandemics that can cause many fatalities.
- Influenza has a really bad predilection of jumping from animals to humans.
- This also is true with coronavirus.
- Some viruses may live in an animal for many years, literally 100 years, and a whole generation or two of humans may have passed by without ever seeing that virus. In that case, there’s no immunity in the whole world’s population. COVID-19 came out of bats.
- We don’t know if next year will be worse. It depends on the number of people infected. We do not have enough testing and some people, unclear how many, have mild cases of COVID-19 infection and may well become immune.
- The SARS virus, which also is a coronavirus, is very closely related to COVID-19. Like COVID-19, the SARS virus jumped from bats into humans in China. SARS had a nine percent mortality rate, pretty disastrous. As a point of comparison, present-day flu is 0.1 percent mortality. COVID-19 is somewhere between 1 percent to 2 or 3 percent.
- But SARS had one thing that was very different from COVID-19. It only spread after people showed symptoms, when you coughed and you were very sick, when you literally went to the hospital. It didn’t spread in the greater population. That’s the reason SARS stopped in a few years.
- In 2012, another coronavirus jumped from camels to humans—that was MERS. MERS is a coronavirus that comes from the Middle East—the acronym is Middle Eastern Respiratory Syndrome. It had a horrendous mortality rate, 50 percent. It never got out of the Middle East. By 2014—just two years later—it stopped. It had such a high mortality rate that people were dying, and you don’t transmit after you’re dead. It requires active infection to transmit.
- COVID-19 takes less virus to infect us, and it has a long latent period with no symptoms so it can spread in a population. Also, unlike flu, coronaviruses can combine with one another, inserting foreign genetic information into its chromosome and changing the properties of the virus.
- COVID-19 seems to have affected people in very different ways. One person can have the virus and not have many symptoms at all. Another person gets sick and dies.
- The good news is that COVID-19 doesn’t mutate very much. It only has a single chromosome. So, there are fewer combinations, and no segregation of chromosomes.
- Viruses come in through your mouth and your nose and get down to your lungs and in your tissue and in the pharynx. It has to get into a cell to replicate because it’s a parasite.
- At the cellular level, coronaviruses have spikes that attach the virus to a cellular protein.
- the protein that COVID19 binds to—it’s the same one that SARS binds to. The protein is called ACE-2 and it coordinates the functioning of your heart and your kidneys.
- That means it takes less virus to infect a cell. It is a much more efficient virus in spreading than SARS was or even influenza is.
- If it settles in the lungs as pneumonia. The immune system attacks the virus-infected cells and kills your lung cells, the epithelial cells of the lining of the tubes to the lungs, and the lungs themselves. Then the lungs fill up with fluids, and that’s a pneumonia. Your oxygen intake is compromised, and eventually one could die from that.
- One of the genes of COVID-19 is an enzyme called a protease.
- When the gene was sequenced, it looked a bit like a human immunodeficiency virus protease gene—the HIV gene, that causes AIDS—for which we have a drug.
- So, that drug has been tried. And it does inhibit the coronavirus enzyme, but not as well as you’d like. So, better inhibitors are being made right now. Maybe there could be a pill that would stop the virus from replicating and stop the pathology.
- There are certain cancer therapies that target a tumor, without killing healthy cells and that therapy may be able to be repurposed for COVID-19.
- it’s possible to take from the patient a cell that confers immunity to viruses or even cancers. That cell, called a T-cell, is modified in the laboratory to “see” the cancer cell as foreign, and then is reintroduced into the cancer patient, where it kills the tumor. But, one side effect is, the T-cell ends up killing some healthy cells, due to a hormone called IL-6. To prevent killing healthy cells, an antibody directed against the IL-6 receptor is also administered and the patient no longer shows the autoimmunity.
- Some people think giving the anti-IL-6 receptor antibody to COVID-19 patients could work in the same way, which would prevent the pneumonia that kills patients.
- Vaccines currently being developed
- There are two ways to test for this virus.
- One way is to test for the virus directly.
- there’s a better way to test the population at large, the whole population--to look for antibodies. If you have been exposed to the virus and it replicates you make antibodies against it. We can test for that. You could prick your finger and get a drop of blood.
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