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Infographics Virus of the Week

West Nile Virus: Virus of the Week

This week on virus of the week is West Nile Virus, another single stranded RNA virus belonging to the flavivirus family! Learn more about other dengue and tick-bourne encephalitis virus!

Taxonomy

Etymology

  • WNV was first isolated from a febrile patient from the West Nile district of Northern Uganda in 1937, (Smithburn et al., 1940).
  • Following naming conventions of the time it was called WNV.

Hosts: What carries WNV?

  • Natural hosts of WNV are mosquitoes and birds, (Jerzak et al., 2005).
  • Culex mosquitoes are particularly important for WNV transmission into humans!
  • Humans are ‘dead end hosts’ – meaning we don’t transmit back to mosquitoes.

Cell Tropism: Which cells can WNV infect?

Vector: What transmits WNV to humans?

  • Culex mosquitoes transmit to humans.
  • This includes: Culex pipiens, C. restuans, C. salinarius, C. quinquefasciatus, C. nigripalpus, C. erraticus and C. tarsalis.

Pathology: What does it do to us?

  • 80 % of infections are asymptomatic.
  • The majority of symptomatic patients experience a weeklong fever.
  • West Nile neuroinvasive disease (WNND) occurs in less than 1 % of infections.

It describes multiple syndromes:

  • West Nile meningitis (WNM)
  • West Nile encephalitis (WNE)
  • West Nile poliomyelitis (WNP)

Did you know?

Men are more likely to experience WNND!

References

  • Brown, A. N., Kent, K. A., Bennett, C. J., & Bernard, K. A. (2007). Tissue tropism and neuroinvasion of West Nile virus do not differ for two mouse strains with different survival rates. Virology, 368(2),422–430. https://doi.org/10.1016/j.virol.2007.06.033.
  • Byas, A. D., & Ebel, G. D. (2020). Comparative pathology of West Nile Virus in humans and non-human animals. Pathogens, 9(1). https://doi.org/10.3390/pathogens9010048.
  • Jerzak, G., Bernard, K. A., Kramer, L. D., & Ebel, G. D. (2005). Genetic variation in West Nile virus from naturally infected mosquitoes and birds suggests quasispecies structure and strong purifying selection. The Journal of General Virology, 86(Pt 8), 2175–2183. https://doi.org/10.1099/vir.0.81015-0.
  • Kilpatrick, A. M., LaDeau, S. L., & Marra, P. P. (2007). Ecology of West Nile Virus Transmission and Its Impact on Birds in the Western Hemisphere. The Auk, 124(4), 1121–1136. http://www.jstor.org/stable/25150376.
  • Petersen, L. R., Brault, A. C., & Nasci, R. S. (2013). West Nile virus: review of the literature. JAMA, 310(3), 308–315. https://doi.org/10.1001/jama.2013.8042.
  • Smithburn, K. C., Hughes, T. P., & Burke, A. (1940). A neurotropic virus isolated from the blood of a native of Uganda. The American Journal of Tropical Medicine, 20, 471–497.
Engineering Infographics

Metrology 101: or how ‘x’ is my piece of ‘y’?

Written by Dr Lewis Newton

Metrology

The science of measurement

In many scientific disciplines, not least your daily life, there is often a need for measurement. In many ways, it is the cornerstone of the scientific method – although this may be bias coming from a Metrologist!

For us metrologists, we are concerned with everything to do with measurement. From the 7 SI units (mass, length, time, etc.) to the instruments that measure them!

Uncertainty

Think of it as confidence in our results – or more positively, certainty!

While it all sounds negative, you’ll often see this in the form of simple “±” with your result, and it’s just a metrologists way of admitting that the world isn’t perfect.

Uncertainty and it’s calculation is all about picking apart the things that have contributed to the value you get for your measurement. These errors can be:

  • Forgetting to start from zero – happens more often than you think!
  • Differences between your repeats – repeatability
  • Temperature changes – materials can shrink/grow a couple of nanometres!

Being highly uncertain isn’t bad! I’m sure you can forgive your scales at home for not being as certain as CERN!

It’s just always better to know your uncertainty in a measurement result.

Système international (d’unités)

Ooo la la: This is what SI stands for! The International System of Units

They are realised by the various national laboratories in different countries (NPL in the UK) – from whom we all check our lengths, masses, etc. are the same as theirs!

The metre is the length of the path travelled by light in vacuum during a time interval of 1/299 792 458 of a second.

To realise it: NPL fires a laser and measures how fast it travels – in a super controlled way!

Traceability

In short, even your ruler is connected to the speed of light…

If you think of metrology as a pyramid, the thing you want to measure is at the bottom; you don’t need it to be super certain – like 0.10000 ± 0.00001 m, but you do want the unit you are using to be the same one as everyone else! – you want to be traceable to the definition of the metre at the top of the pyramid!

So you have connected measurements that link them all together – this is calibration.

Calibration

This is a word that needs some clarity! Especially in metrology

While it has other uses in wider day to day life, in metrology we aren’t adjusting ‘the scales’ when we calibrate! This is more of a correction.

Calibration involves comparing the measurement result from your system with a known-value (from a ‘better’ measurement system, which might have uncertainties associated with it!). BUT you can use this knowledge (maybe there’s some systemetic errors?!) to apply corrections!

Further Reading

General sites to learn more:
Books for reference reading:

About the author:

Lewis is a Research Fellow at the University of Nottingham within the Manufacturing Metrology Team. Currently, his research is in the development of optical measurement systems for the measurement of aesthetic surfaces relating to human perception and further investigations into feature-based characterisation pipelines for novel applications.

This is part of our engineering series, find more here.

Infographics Virus of the Week

Tick-bourne encephalitis virus: Virus of the Week

Today we are introducing you in brief to Tick-bourne encephalitis virus, another flavivirus spread by ticks!

Taxonomy

Tick-bourne encephalitis virus (TBEV) is a positive sense single stranded RNA virus, belonging to the flavivirus family. See other flavivirus Dengue here.

Etymology

The name self-explanatory, a virus which is carried by ticks and causes encephalitis! The first recorded case dates back to the 18th century Scandinavian church records (Lindquist & Vapalahti, 2008).

Hosts

  • Ixodes spp. a species of tick, transmits the virus to humans, though the cycle includes birds and deer.
  • Nymphs have reduced host specificity – so are the most important for human transmission!

Cell Tropism

  • The brain.
  • Dendritic cells found in the skin.
  • Neutrophils – a type of immune cell.

Vector

  • Ixodes spp. are responsible for transmission of TBEV to humans.
  • Habitats range from western Europe to the eastern coast of Japan (Lindquist & Vapalahti, 2008).

Did you know?

Recent studies indicate that the thread of TBEV in europe will escalate with climate change as climate change forces the viruses host northwards. (Nah et al, 2020).

References

  • Kuno G, Chang GJ, Tsuchiya KR, Karabatsos N, Cropp CB. Phylogeny of the genus Flavivirus. J Virol. 1998 Jan;72(1) 73-83. doi:10.1128/jvi.72.1.73-83.1998. PMID: 9420202; PMCID: PMC109351.
  • Labuda, M., Austyn, J. M., Zuffova, E., Kozuch, O., Fuchsberger, N., Lysy, J., & Nuttall, P. A. (1996). Importance of localized skin infection in tick-borne encephalitis virus transmission. Virology, 219(2), 357–366. https://doi.org/10.1006/viro.1996.0261
  • Lindquist, L., & Vapalahti, O. (2008). Tick-borne encephalitis. The Lancet, 371(9627), 1861–1871. https://doi.org/10.1016/S0140-6736(08)60800-4
  • Nah, K., Bede-Fazekas, Á., Trájer, A.J. et al. The potential impact of climate change on the transmission risk of tick-borne encephalitis in Hungary. BMC Infect Dis 20, 34 (2020). https://doi.org/10.1186/s12879-019-4734-4
Infographics Virus of the Week

Dengue Virus: Virus of the Week

This week’s virus of the week is Dengue virus! This virus belongs to the Flavivirus genus and has a positive sense, single stranded RNA genome.

Etymology, where does the name come from?

There are several possibilities:

  • Swahili phrase Ka-dinga pepo (cramp like seizure caused by an evil spirit), which potentially originated from the Spanish word ‘dengue’ meaning careful.
  • Alternatively, posture described resembled a ‘dandy’ in English hence ‘dandy-fever’, (Halstead, 2008) .

What are the Hosts of Dengue Virus?

  • Natural cycles exist between Aedes mosquitoes and non-human primates like gorillas.
  • Rarely, this virus emerges into humans!

Cell tropism of Dengue virus – which cells do they infect?

  • Cutaenous Langerhans Dendritic cells – which are found in the skin.
  • Various immune cells! Including Monocytes, macrophages, as well as B-cells and T-cells.
  • Cells in the brain
  • Endothelial cells, which can be found in blood vessels for example.

Transmission

  • Aedes mosquitoes are responsible for Dengue transmission.
  • The most prolific mosquito being Aedes aegypti.

Pathology

There are actually three phases to the Dengue virus infection

Phase 1:

Also known as the febrile phase, where an infected person will have a fever and flu-like symptoms, and potentially a rash. This can last between 3-7 days, and most patients recover after this period.

Phase 2:

Also known as the critical phase, which occurs mainly in children and younger adults. This phase is associated with a vascular leakage syndrome causing low protein and high cell-debris in the blood with fluid around the lungs.

Phase 3:

The recovery phase which can sometimes be associated with another rash.

A second Dengue virus infection is often more severe than the first infection, this is due to a phenomenon known as antibody-dependent enhancement (ADE).

Did you know?

The first suspected cases of Dengue are found in Chinese Medical Textbooks which date back to 992.

References

  • Balsitis, S. J., Coloma, J., Castro, G., Alava, A., Flores,D., McKerrow, J. H., Beatty, P. R., & Harris, E. (2009). Tropism of dengue virus in mice and humans defined by viral nonstructural protein  3-specific immunostaining. The American Journal of Tropical Medicine and Hygiene, 80(3), 416–424.
  • Blackley, S., Kou, Z., Chen, H., Quinn, M., Rose, R. C., Schlesinger, J. J., Coppage, M., & Jin, X. (2007). Primary human splenic macrophages, but not T or B cells, are the principal target  cells for dengue virus infection in vitro. Journal of Virology, 81(24), 13325–13334. https://doi.org/10.1128/JVI.01568-07.
  • Halstead, S. B. (2008). Dengue (Vol. 5). Imperial College Press. https://doi.org/10.1142/p570 Holmes, E. C., & Twiddy, S. S. (2003). The origin, emergence and evolutionary genetics of dengue virus. Infection, Genetics and Evolution, 3(1), 19–28. https://doi.org/10.1016/S1567-1348(03)00004-2.
  • Jessie, K., Fong, M. Y., Devi, S., Lam, S. K., & Wong, K. T. (2004). Localization of dengue virus in naturally infected human tissues, by  immunohistochemistry and in situ hybridization. The Journal of Infectious Diseases, 189(8), 1411–1418. https://doi.org/10.1086/383043.
  • King, A. D., Nisalak, A., Kalayanrooj, S., Myint, K. S., Pattanapanyasat, K., Nimmannitya, S., & Innis, B. L. (1999). B cells are the principal circulating mononuclear cells infected by dengue virus. The Southeast Asian Journal of Tropical Medicine and Public Health, 30(4), 718–728.
  • Martins, S. de T., Silveira, G. F., Alves, L. R., Duarte dos Santos, C. N., & Bordignon, J. (2012). Dendritic cell apoptosis and the pathogenesis of dengue. Viruses, 4(11), 2736–2753. https://doi.org/10.3390/v4112736
  • Mota, J., & Rico-Hesse, R. (2011). Dengue virus tropism in humanized mice recapitulates human dengue fever. PloS One, 6(6), e20762. https://doi.org/10.1371/journal.pone.0020762.
  • Scott, T. W., & Morrison, A. C. (2010). Vector Dynamics and Transmission of Dengue Virus: Implications for Dengue Surveillance and Prevention Strategies BT  – Dengue Virus (A. L. Rothman (ed.); pp. 115–128). Springer Berlin Heidelberg. https://doi.org/10.1007/978-3-642-02215-9_9.
  • Weaver, S. C., Charlier, C., Vasilakis, N., & Lecuit, M. (2018). Zika, Chikungunya, and Other Emerging Vector-Borne Viral Diseases. Annual Review of Medicine, 69, 395–408. https://doi.org/10.1146/annurev-med-050715-105122

COVID-19 Infographics

Misinformation vs disinformation, what’s the difference?

Misinformation vs disinformation, what’s the difference? This infographic briefly defines the difference between misinformation and disinformation. Both misinformation and disinformation refers to information that is not factually correct, however, misinformation may be spread due to poor understanding of the subject, or just by mistake. Disinformation is when incorrect information is spread on purpose.

Misinformation

Is factually incorrect information – regardless of intent. It may be a mistake, or a misinterpretation of data.

Disinformation

Is the deliberate spreading of false information. Someone who spreads disinformation is doing so knowingly.

If you’re not sure, don’t share.

Use our Misinformation Toolkit to help navigate through misinformation and disinformation online.

COVID-19 Infographics

The Misinformation Toolkit

So. You’ve seen something you think is misinformation. What do you do?

Here is The Science Social Misinformation Toolkit.

Not sure? Don’t share!

Not sure, don’t share is our mantra.

If you have second thoughts about something you’re reading online, do not continue to share it.

The wrong advice or information can do more harm than good. Sharing because you think it could be useful knowledge without actually checking could result in someone taking potentially harmful action.

Although it is an extreme example, there were reports only weeks ago that ‘drinking bleach could rid you of coronavirus’. Whilst many of us may consider it common sense not to follow this advice, we should be mindful not to share it.

Fact check…

Fake news or misinformation is often propagated because it looks legitimate. Don’t be fooled by a credible name drop!

Often this could be:

“a friend of mine who works at the hospital received this email…” or “this is an NHS letter…”.

If the information is legitimate, it will be easily accessible via the online resources of the named institution, be that NHS, PHE, Gov.uk or University websites.

Check for yourself before taking further action.

Speak up!

There is nothing wrong with questioning the source.

This is what science is all about!

  • It is good practice in scientific research to ask what the evidence is where it came from and who produced it before drawing any conclusions.

Once you’ve spotted misinformation you can start asking these questions yourself if you feel comfortable doing so. Most people will engage with you if approached in a diplomatic and considerate way.

It is important to always be respectful of another persons views, even if you don’t agree!

It’s all about you

Even if you can’t find out more information about a source or identify it’s credibility, your questioning alone is the first step towards stopping the spread and uptake of misinformation.

If you’re not sure, don’t share.

The best way to protect yourself and your loved ones is to follow Public Health guidelines and stay up to date with any amendments to the existing advice.

Related: Misinformation: Believe, Share, Avoid?

Don’t forget to share The Misinformation Toolkit!

Blog Virology Virus of the Week

Introducing: Virus of the Week

Did you know that there are over 1031 viruses on this earth…? That’s ten nonillion?!

You didn’t?

This is Virus of the Week:

The Science Social has made it their mission to introduce a virus each week to help raise general understanding of virology. We don’t think we will get through all the viruses through this series, just a select few.

Here are some of the things that you will learn about each virus that we chose to present to you each week:

  • Taxonomy
  • Etymology
  • Hosts
  • Cell tropism
  • Transmission
  • Pathology
  • “Did you know…?”
  • And of course, a reference list from peer reviewed articles so you can be assured, we are not making it up!

But wait… I don’t know what any of that means…

Taxonomy:

Taxonomy is a tool used by scientists to classify all living things. Think of it as a bit like a really big, detailed family tree which shows you how closely related each living thing is. This was developed by a Swedish botanist named Carolus Linnaeus back in the 18th century. In short, all living things are grouped into 7 Kingdoms of life; e.g. Animalia, Plantae, Fungi, Chromista, Protozoa, Archaea and Bacteria. Each Kingdom of life are then split further into Phylum > Class > Phylum > Order > Family > Genus > Species.

The scientific classification of a human is:

Domain: Eukaryota
Kingdom: Animalia
Phylum: Chordata
Class: Mammalia
Order: Primates
Family: Hominidae
Genus: Homo
Species: sapiens

I’m sure you are all familiar with Homo sapiens, well this is how we, as humans, fit into the taxonomy hierarchy.

Live Science give a good overview of taxonomy here!

The Taxonomy of Viruses though?!

The International Committee on Taxonomy of Viruses (ICTV) are responsible for developing, refining and maintaining a universal virus taxonomy. You can find more out about them here.

Etymology:

This one literally means, where did the name come from.

Hosts:

We will be discussing what hosts the virus of the week can replicate in. We will be looking at viruses where the humans are the main host, but also others too.

Cell tropism:

This is a fancy scientific way of saying, which cells in the body (or organism) the virus is “attracted” too. For example, this virus infects mainly these cells.

Transmission:

How is the virus transmitted?! Through the air? A vector (for example a mosquito or a tick…?), contaminated food or water?

Pathology:

What does the infection of this particularly look like in the form of disease?

Did you know?:

We thought we would throw in a fun fact… just to attempt at making this interesting.

Remember we have a virology section on our blog which you can find here!

We hope you enjoy virus of the week – we are really excited to share this with you!

Blog Guest Blog

One Health, One Medicine: what is it?

Written by Emily Clarke @E_Clarke_Sci @LabPeffers

One medicine promotes collaboration between doctors, vets, scientists and other medical professionals so veterinary and human medicine can evolve and improve so both benefit from equal medical progress (1).

One health focuses specifically on how the health of people is closely connected to the health of animals and our shared environment (2).

History of One Health, One Medicine

The concept of one medicine and one health has been around for a LONG time…

It was first referred to by Rudolf Virchow, regarded as the father of modern pathology (3) whose discoveries on Trichinella spiralis in pork led to valuable public health measures.

Even today Vets are heavily involved in food production to stop contamination or disease entering the human food chain. Virchow was one of the first to coin the term “zoonosis” and proclaimed that there should be no dividing line between human and animal medicine (4,5).

Sir William Osler, regarded as the father of modern medicine,was another key figure in promoting one medicine, as he taught medical students at McGill College and veterinary students at the Montreal Veterinary College in the 1870s.

Demonstrating how one subject area could co exist and benefit the other. Osler published on the relation of animals to man and promoted comparative pathology and the One Medicine Concept (4,5).

In the 20th century, Calvin Schwabe coined the concept of “one medicine” in a modern age, recognising that there is very little difference between human and veterinary medicine and both disciplines can contribute to the development of each other (4).

Zoonosis = Disease that can transmit between humans and animals.

What are the applications of one health, one medicine?

If you have seen the bionic vet  then you already know a fantastic example of one medicine. Professor Noel Fitzpatrick routinely uses human medical principles for orthopaedic surgery to conduct the incredible surgeries he does on the nation’s beloved pets!

Further more general applications include:

Why should we care?

  • It is more ethical – both animals and humans are benefitting from this kind of research.
  • There is potential for faster medical progress.
  • This type of research could result in more animal and humans lives saved.
  • Better quality of life for humans and animals is achieved.
  • Ultimately, this type of research has an even bigger impact.

References

  1. https://www.humanimaltrust.org.uk/who-we-are
  2. https://www.cdc.gov/onehealth/basics/index.html
  3. Cardiff, R.D., Ward, J.M. and Barthold, S.W., 2008. ‘One medicine—one pathology’: are veterinary and human pathology prepared?. Laboratory investigation, 88(1), pp.18-26.
  4. Zinsstag, J., Schelling, E., Waltner-Toews, D. and Tanner, M., 2011. From “one medicine” to “one health” and systemic approaches to health and well-being. Preventive veterinary medicine, 101(3-4), pp.148-156.
  5. Kahn, L.H., Kaplan, B., Monath, T.P. and Steele, J.H., 2008. Teaching “one medicine, one health”. The American journal of medicine, 121(3), p.169.

More guest blogs here:

Blogs written by DiMeN DTP students:

Infographics Uncategorized

Tissue-specific tolerance in fatal COVID-19

COVID-19 fatality: invader vs the immune system.

Our new blog provides a breakdown of a paper in preprint from the ICECAP consortium.

A team of pathologists, virologists and clinicians found that the virus was detectable in multiple organs and that there was a mismatch between virus presence and inflammation. This suggests that different tissues in the body have a different tolerance for the virus.

The study is a post-mortem study, where those who have died in hospital from COVID-19 were examined to determine mechanisms of the disease. Post-mortem examinations provide an opportunity to study the whole body in a way which is not possible during life, providing insight into disease and clinical characteristics of disease.

This research reveals how immune mediated organ inflammation and injury may be a key driver of fatality.

The study concludes that:

  • There is a mismatch between the presence of SARS-CoV-2, tissue inflammation and organ dysfunction
  • There is a tissue specific tolerance to SARS-CoV-2
  • Death is a consequence of immune mediated organ inflammation and injury

Key findings

The Coronavirus was found in multiple organs within patients who died from COVID-19.

Most commonly in the lungs but also in other parts of the body, such as the heart, muscle and the gastrointestinal tract. In some cases, virus was detected in the liver, kidney and other organs.

Inflammation was not observed in non-pulmonary organs

Interestingly, virus that was detected outside of the lung, was usually not associated with local inflammation, despite frequent detection of viral RNA and protein. This was the case for tissues such as the intestine, liver and kidney.

Inflammation was identified in lung tissue

Lung damage consisted of significant injury to the alveoli (the part of the lung involved in uptake of oxygen), the identification of blood clots and inflammation of pulmonary blood vessels. Interestingly again, there was not a consistent association between the presence of viral RNA and either the presence or nature of the inflammatory response within the lung.

Abnormalities of the blood and the immune system

Abnormalities were found in the blood and immune system; two key cell types are discussed:

  • Macrophages – an immune cell that is involved in sensing and responding to pathogens and tissue repair.
  • Plasma cells – cells involved in producing antibodies.

Abnormal macrophages and an increased number of abnormal plasma cells were identified in the organs of the immune system. Within damaged lung tissues, the researchers identified that macrophages and macrophage-like cells were in high numbers.

The consequence of these abnormalities is currently unknown; however, this finding provides a direction for COVID-19 researchers and future studies.

Note: this article is still awaiting peer review.

Read our blog to find out more!

Here: https://www.thesciencesocial.com/2020/08/17/covid-19-fatality/. Follow us on Instagram, Twitter and Facebook!

Blog COVID-19 Research Summaries

COVID-19 fatality: Invader vs the immune system

Written by Rebekah Penrice-Randal

COVID-19 fatality may be associated with damage caused by our immune system as opposed to direct damage from the virus. Dexamethasone, a drug that has recently proved to reduce fatality in severely ill COVID-19 patients, suggests that inflammation plays a direct role in patient outcomes.

Is the inflammation caused be the virus itself, or the body’s immune system? Currently, this is unknown.

For a quick recap on the immune system: visit our infographic here.

The ICECAP consortia have released a preprint in MedRxiv that may hold the answer to this question. Tissues from 12 individuals who have died from COVID-19 in hospital were analysed by a team of pathologists, clinicians and virologists to determine where the virus was found and whether this corresponded to where inflammation was found.

Who are ICECAP?

ICECAP: Inflammation in COVID-19-Exploration of Critical Aspects of Pathogenesis.

“ICECAP was established as a rapid response to the COVID-19 pandemic. We collect and analyse tissue samples to understand COVID-19 and other fatal diseases, contributing to finding tests and treatments for these conditions.”

Tissue-specific tolerance in fatal Covid-19 is the first research output from this consortia.

Definitions of key words:

  • Inflammation: a local immune response to cellular injury.
  • Post-mortem: the study of the deceased.
  • Immune system: a system of the body that fights off infection and disease, including white blood cells, antibodies and the organs that produce these cells.
  • Macrophage: a specialised immune cell involved in the innate immune response.
  • Plasma cell: an immune cell that produces antibodies that make up the adaptive immune response.
  • Pulmonary: relating to the lungs.

Key findings

The Coronavirus was found in multiple organs within patients who died from COVID-19.

Most commonly in the lungs but also in other parts of the body, such as the heart, muscle and the gastrointestinal tract. In some cases, virus was detected in the liver, kidney and other organs.

Inflammation was not observed in non-pulmonary organs

Interestingly, virus that was detected outside of the lung, was usually not associated with local inflammation, despite frequent detection of viral RNA and protein. This was the case for tissues such as the intestine, liver and kidney.

Inflammation was identified in lung tissue

Lung damage consisted of significant injury to the alveoli (the part of the lung involved in uptake of oxygen), the identification of blood clots and inflammation of pulmonary blood vessels. Interestingly again, there was not a consistent association between the presence of viral RNA and either the presence or nature of the inflammatory response within the lung.

Abnormalities of the blood and the immune system

Abnormalities were found in the blood and immune system; two key cell types are discussed:

  • Macrophages – an immune cell that is involved in sensing and responding to pathogens and tissue repair.
  • Plasma cells – cells involved in producing antibodies.

Abnormal macrophages and an increased number of abnormal plasma cells were identified in the organs of the immune system. Within damaged lung tissues, the researchers identified that macrophages and macrophage-like cells were in high numbers.

The consequence of these abnormalities is currently unknown; however, this finding provides a direction for COVID-19 researchers and future studies.

Conclusions

The take home message from this research is that different tissues appear to have a different tolerance to the virus. Inflammation and damage to organs are likely to be extensively mediated by the body’s own immune system, and drives outcome from disease.

A note on preprint and peer review:

This research has not gone through the peer review process yet – visit our posts on peer review here.

Interested in communicating your research to a lay audience? Get in touch at info@thesciencesocial.com

Thank you to Dr Chris Lucas, an ICECAP investigator and co-author of the original article for permission to write this blog, and for the valuable comments.

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