Category: Diseases, Syndromes and Conditions

Categories : Diseases, Syndromes and Conditions New Compounds and TreatmentsTags :

New Antibody Treatment for Crimean-Congo Haemorrhagic Fever

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Deer tick (Ixodes scapularis). Photo by Erik Karits on Unsplash

Working with international colleagues, US Army scientists have developed and tested an antibody-based therapy to treat Crimean-Congo haemorrhagic fever virus (CCHFV). 

The deadly virus is carried by ticks and has a high mortality rate, killing up to 60% of those infected. Their findings are published in the journal Cell.

The researchers characterised the human immune response to natural CCHFV infection by using blood samples donated by disease survivors. They were able to identify several potent neutralising antibodies that target the viral glycoprotein–a viral component which has a key role in disease development. A number of of these antibodies, administered individually or in combination, successfully protected mice from CCHFV when exposed to the virus after antibody administration.

In order to treat mice that had already been infected with the virus, the team created ‘bispecific’ antibodies that combined potency with the ability to bind to two different sites on the CCHFV glycoprotein. One of these bispecific antibodies, called DVD-121-801, overcame CCHFV infection in mice with just a single dose administered 24 hours after challenge with live virus.

DVD-121-801 as a potential therapeutic for human patients, according to co-first author Andrew H. Herbert, Ph.D., of the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID).

CCHFV is the most prevalent tick-borne virus that causes human disease, and is endemic in countries across Europe, Asia, and Africa. CCHF occurs most frequently among agricultural workers following the bite of an infected tick, and to a lesser extent among slaughterhouse workers exposed to the blood and tissues of infected livestock and medical personnel through contact with the body fluids of infected patients. In spite of its high lethality and widespread distribution, there are no vaccines or specific treatments for it. It has been designated a priority pathogen by the World Health Organization.

Study co-first author Andrew H Herbert, PhD, US Army Medical Research Institute of Infectious Diseases, said: “Rodent models of CCHFV infection are useful in testing and down-selecting neutralising antibodies. However, to advance a lead candidate for therapeutic use, it will be necessary to conduct studies in larger animal models that more faithfully recapitulate human disease.”

Source: Medical Xpress

Journal information: J. Maximilian Fels et al, Protective neutralizing antibodies from human survivors of Crimean-Congo hemorrhagic fever, Cell (2021). DOI: 10.1016/j.cell.2021.05.001

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China Reports First Human Infection of the H10N3 Avian Flu Strain

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Image by Arek Socha from Pixabay

On Tuesday, China reported the world’s first human infection of the H10N3 avian flu strain but said the risk of its widespread transmission among people was low.

In the eastern city of Zhenjiang, a 41-year-old man was admitted to hospital with fever symptoms on April 28 and a month later was diagnosed with H10N3, China’s National Health Commission (NHC) said in an online statement.

The NHC said that “The risk of large-scale spread is extremely low,” and that the man was in a stable condition with his close contacts having reported no “abnormalities”.

The health body described H10N3 as being low pathogenic, ie less likely to cause death or severe illness, in birds. It said there had been no human cases of H10N3 previously reported anywhere in the world.

A number of strains of bird flu have been found among animals in China but mass outbreaks in humans are rare.

Five waves of the H7N9 influenza epidemic occurred in China between March 2013 and September 2017. Low pathogenicity H7N9 dominated in the first four waves, whereas highly pathogenic H7N9 influenza emerged in poultry and spread to humans during the fifth wave, causing widespread concern.  

H7N9 has infected 1668 people and claimed 616 lives since 2013, according to the United Nations’ Food and Agriculture Organization. In the wake of recent avian flu outbreaks in Africa and Eurasia, the head of China’s Centre for Disease Control and Prevention last week urged closer surveillance in poultry farms, markets and wild birds.

COVID was first detected at a wet market with food and live animals in the central Chinese city of Wuhan in late 2019. This is where, according to the most likely scenario from the WHO report on the virus’ origins, it is thought that the SARS-CoV-2 virus first jumped from animals to humans. 

Source: Medical Xpress

Categories : Diseases, Syndromes and Conditions GeneticsTags :

Gene Drive to Control Mosquito-borne Disease a Step Closer

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Image source: Ekamalev at Unsplash

Scientists have developed a set of tools that will help create a gene drive to control mosquito-borne diseases such as the West Nile virus, which has received less attention than controlling mosquitoes that transmit malaria.

Since the advent of CRISPR genetic editing revolution, scientists have been working to use the technology to develop gene drives that target pathogen-spreading mosquitoes such as Anopheles and Aedes species, which spread malaria, dengue and other life-threatening diseases.

Much less genetic engineering work has focused on Culex genus mosquitoes, which spread devastating afflictions stemming from West Nile virus, as well as other viruses such as the Japanese encephalitis virus (JEV). Culex mosquitoes are a significant health risk in Africa and Asia, where they transmit the worm causing filariasis, a disease that can lead to a chronic debilitating condition known as elephantiasis.

University of California San Diego scientists have now developed a number of genetic editing tools that will help create a gene drive designed to stop Culex mosquitoes from spreading disease. Gene drives are designed to spread modified genes, in this case those that disable the ability to transmit pathogens, throughout the targeted wild population. The new study is published in the journal Nature Communications,

The researchers developed a Cas9/guide-RNA expression ‘toolkit’ designed for Culex mosquitoes. Since so little genetic engineering work has been done on Culex mosquitoes, the researchers were required to develop their toolkit from scratch, starting with a careful examination of the Culex genome.

“My coauthors and I believe that our work will be impactful for scientists working on the biology of the Culex disease vector since new genetic tools are deeply needed in this field,” said Gantz, an assistant research scientist in the Division of Biological Sciences at UC San Diego. “We also believe the scientific community beyond the gene drive field will welcome these findings since they could be of broad interest.”

The researchers also demonstrated the applicability of their tools in other insects.

“These modified gRNAs can increase gene drive performance in the fruit fly and could potentially offer better alternatives for future gene drive and gene-editing products in other species,” said Gantz.

Gantz and his colleagues have now tested their new tools to ensure proper genetic expression of the CRISPR components and are now on the verge of applying them to a gene drive in Culex mosquitoes. This could be used to stop pathogen transmission by Culex mosquitoes, or alternatively employed to suppress the mosquito population to prevent biting.

Source: University of California San Diego

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SA Study Finds That Influenza is Widely Spread by Asymptomatic Cases

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Image by Arek Socha from Pixabay

A new study investigated the prevalence and transmission of influenza in rural and urban South Africa communities.

The study was conducted by the National Institute for Communicable Diseases (NICD), Perinatal HIV Research Unit (PHRU), WITS Agincourt HDSS in partnership with the US Centers for Disease Control and Prevention (CDC), who also funded the study. 

Influenza, a communicable viral disease caused by a spectrum of influenza viruses, affects the upper respiratory tract, including upper and lower respiratory passages. The virus can be transmitted in droplets from coughing, talking or sneezing, and through touching contaminated surfaces.

Researchers enrolled 100 rural and urban households in South Africaeach year and observed them for 10 months. Systematic twice-weekly nasopharyngeal sampling of all household members were conducted, with samples tested by polymerase chain reaction (PCR) for influenza. A total of 81 430 samples were collected from 1116 participants in 225 households, out of which 917 (1%) tested positive for influenza and 79% of households (178/225) had ≥1 influenza-positive individual.

The burden of was high in a rural and an urban African setting, the study revealed, with over three-quarters of households and more than one in three individuals experiencing at least one flu infection each year. It is important to note that the flu incidence risk was similar between the rural and urban areas who participated in the study. The study also showed that recurring flu infections in the same annual flu epidemic, particularly in children, were a common occurrence, accounting for 15% of those infected. Young children also experienced the highest burden of flu infection and symptomatic illness — and compared to other age groups, they were more likely to spread the flu to others in their household.

In addition, the study also revealed that slightly over half of the flu infections were symptomatic. Asymptomatic individuals were also able to spread flu, transmitting the flu to approximately 6% of household contacts. For this reason, authors of the study believe asymptomatic infections to be an important driver of flu transmission.

Medically attended influenza-associated influenza like illness (ILI), defined as a fever and cough as captured by the World Health Organization-recommended flu surveillance programs, suggests the prevalence of flu within communities may be much higher than observed at healthcare facilities. Understanding the community burden and transmission of seasonal influenza is crucial for vaccination programmes and non-pharmaceutical interventions, as well as pandemic preparedness.

In conclusion, the study provides important data on the community burden of flu and transmission thereof in an African setting, a topic that hasn’t been adequately explored. It also contributes important findings relating to symptomatic and asymptomatic flu transmissions, and has implications for the use of non-pharmaceutical interventions and vaccination strategies that target children.

A similar study to examine the burden and transmission of SARS-CoV-2 in the same communities including the role of asymptomatic infections in the spread of SARS-CoV-2 was initiated in July 2020 and results of this study are expected in the coming months.

Source: National Institute for Communicable Diseases

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New Way to Compare Effectiveness of Tuberculosis Treatments

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E. Coli bacteria. Image by CDC

A new study published in Nature Communications provides an important new basis for comparing the varying effectiveness of tuberculosis treatments.

Tuberculosis is a ancient disease caused by the bacterium Mycobacterium tuberculosis (Mtb) and aside from the COVID pandemic, is still the leading infectious cause of death globally, killing 1.2 million people each year. The availability of a new way to evaluate treatments can save lives.

In the study, the researchers aimed to provide a new perspective on assessing the effectiveness of tuberculosis drugs.

“A key roadblock that holds back new tuberculosis treatments is our current inability to accurately measure how effectively different treatments shorten the time needed to cure tuberculosis,” said lead author Nicholas Walter, MD, Ph.D., associate professor at the University of Colorado Anschutz Medical Campus. “Without improved tools to measure and compare the effectiveness of drug treatments, the evaluation and roll-out of new combination drug treatments will continue to proceed slowly.”

“In the past, the effectiveness of tuberculosis treatment has been judged by estimating the burden of the pathogen M. tuberculosis as enumerated via culture based approaches. This historical method correlates poorly with what we care about most, which is whether tuberculosis patients are durably cured,” added co-first author Gregory Robertson, PhD, assistant professor at Colorado State University.

By Vossman - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=6865434
Structure and shape of the E.coli 70S ribosome. The large 50S ribosomal subunit (red) and small 30S ribosomal subunit (blue) are shown with a 200 Ångstrom (20 nm) scale bar.

The researchers measured the extent to which drugs interrupt the synthesis of ribosomal RNA, which is needed for the protein-making machinery of the bacterium. They found that drugs and drug regimens that treat tuberculosis faster inhibit Mtb rRNA synthesis more than less potent drugs and regimens. Their resulting new measure, called the rRNA synthesis (RS) Ratio is a useful molecular metric of drug activity based on a key microbial physiologic property rather than a simple measure of reducing bacterial burden.

“The RS Ratio gives us a readout of drug effect that opens a new era in understanding antibiotics. Measuring a key physiologic property of pathogens provides an innovative way of thinking beyond conventional measures of bacterial burden,” said senior author Martin Voskuil, PhD, associate professor at the University of Colorado Anschutz Medical Campus.

“The RS Ratio can enable more intelligent design and evaluation of candidate drug combination regimens, accelerating the development of treatments that can cure tuberculosis faster. This has crucial implications for combatting the global tuberculosis epidemic,” addrf co-author Payam Nahid, MD, MPH, professor and director of the University of California San Francisco Center for Tuberculosis.

Source: Medical Xpress

Categories : Diseases, Syndromes and Conditions New Compounds and TreatmentsTags :

New Antimalarial Compound Traps Parasites in Cells

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Photo by Егор Камелев on Unsplash

To combat the growing resistance of malaria to current treatments, researchers at the Francis Crick Institute and the Latvian Institute of Organic Synthesis have designed a new antimalarial compound which interrupts the malaria parasite life cycle by trapping them in their host cells.

While drugs and mosquito control have reduced levels of malaria over recent decades, with malaria being effectively wiped out in North America by the 1950s, the parasite still kills over 400 000 people every year, 90% of whom live in sub-Saharan Africa. It has now developed resistance to many existing antimalarial drugs, meaning new treatments that work in different ways are urgently needed.

If we can effectively trap malaria in the cell by blocking the parasite’s exit route, we could stop the disease in its tracks and halt its devastating cycle of invading cells.
Mike Blackman

The researchers developed an array of compounds designed to prevent the parasites bursting out of blood cells, a vital replication step. One compound in particular was found to be very effective in human cell tests.

“Malaria parasites invade red blood cells where they replicate many times, before bursting out into the bloodstream to repeat the process. It’s this cycle and build-up of infected red blood cells which causes the symptoms and sometimes fatal effects of the disease,” says Mike Blackman, lead author and group leader of the Malaria Biochemistry Laboratory at the Crick.  

“If we can effectively trap malaria in the cell by blocking the parasite’s exit route, we could stop the disease in its tracks and halt its devastating cycle of invading cells.”

Blocking the parasite’s emergence

The compound works by blocking an enzyme called SUB1, needed for them to burst out of cells. Current antimalarials kill the parasite within the cell, so the researchers hope this alternative drug action will overcome the resistance the parasite has acquired.

The compound can penetrate both the cell wall and the compartment within where the parasites reside.

The researchers are further refining the compound making it smaller and more potent. Further tests are needed before it can be trialled in humans.

Study author Chrislaine Withers-Martinez and researcher in the Malaria Biochemistry Laboratory, said: “Many existing antimalarial drugs are plant derived and while they’re incredibly effective, we don’t know the precise mechanisms behind how they work. Our decades of research have helped us identify and understand pathways crucial to the malaria life cycle allowing us to rationally design new drug compounds based on the structure and mechanism of critical enzymes like SUB1.

“This approach, which has already been highly successful at finding new treatments for diseases including HIV and Hepatitis C, could be key to sustained and effective malaria control for many years to come.” 

Source: Francis Crick Institute

Categories : Diseases, Syndromes and Conditions ImmunologyTags :

Sepsis Leaves a Dangerous Imprint in Immune System

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E. Coli bacteria. Image by Gerd Altmann from Pixabay

New research suggests that sepsis can cause alterations in the functioning of defence cells that persist even after the patient is discharged from hospital.

This cellular reprogramming creates a disorder the authors term ‘post-sepsis syndrome’, symptoms of which include frequent reinfections, cardiovascular alterations, cognitive disabilities, declining physical functions, and poor quality of life.This explains why so many patients who survive sepsis die sooner after hospital discharge than patients with other diseases or suffer from post-sepsis syndrome, immunosuppression and chronic inflammation.

The article reviews studies done to investigate cases of septic patients who died up to five years after hospital discharge.

Sepsis is one of the main causes of death in intensive care units, sepsis is a life-threatening systemic organ dysfunction triggered by the body’s dysregulated response to a pathogen, usually a bacterium or fungus. While fighting the pathogen, the defence system injures the body’s own tissues and organs.

If not caught and treated in time, the condition can lead to septic shock and multiple organ failure. Patients with severe COVID and other infectious diseases have an increased risk of developing and dying from sepsis.

Worldwide, new sepsis cases are estimated to reach some 49 million per year. Hospital mortality from septic shock exceeds 40% globally, up to 55% in Brazil, according to the Sepsis Prevalence Assessment Database (SPREAD) study, conducted with support from FAPESP.

“The massive infection and the accompanying intense immune response with a cytokine outpouring during sepsis may promote irreversible cell metabolic reprogramming. Cell reprogramming is unlikely to occur in leukocytes or bone marrow only. This might happen in several tissues and cells that prompt systemic organ dysfunctions […] Bacteria can transfer genetic material to host cell DNA as eukaryotic cells develop tools to protect themselves against the microorganism invasion. The latter may induce cell biology and metabolic reprogramming that remains even after the infection’s elimination,” the investigators wrote in the article.

According to Raquel Bragante Gritte, joint first author with Talita Souza-Siqueira, one of the hypotheses was that metabolic reprogramming begins in the bone marrow, whose cells acquire a pro-inflammatory profile.

“Our analysis of blood samples from patients even three years after ICU discharge showed that monocytes [a type of defense cell] were activated and ready for battle. They should have been neutral. Monocytes are normally activated only when they are ‘recruited’ to the tissue,” Gritte told Agência FAPESP. Both Gritte and Souza-Siqueira are researchers at Cruzeiro do Sul University (UNICSUL) in the state of São Paulo, Brazil.

The researchers conducted a follow-up study of 62 patients for three years after discharge from the ICU at USP’s University Hospital, analysing alterations in monocytes, neutrophils and lymphocytes, as well as microRNAs, in order to identify prognostic markers and factors associated with post-sepsis syndrome.

“Our hypothesis is that white blood cells conserve a memory of sepsis, which helps explain why patients remain sick after they leave hospital,” said co-author Rui Curi, Professor at UNICSUL, and Director of Butantan Institute.

The investigators suggest that sepsis may create a specific macrophage phenotype that stays active even after hospital discharge. “Cell metabolism reprogramming is also involved in the functions and even generation of the different lymphocyte subsets. Several stimuli and conditions change lymphocyte metabolism, including microenvironment nutrient availability,” they wrote.

The next stage of research will be bone marrow studies to understand how cells are reprogrammed by sepsis. “We think the key to this alteration is in bone marrow,” she said. “However, another possibility is that activation occurs in the blood. We’ll need to do more in-depth research to find answers.”

Source: News-Medical.Net

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How Legionnaire’s Disease Digs In

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A bunker from World War II, emulating how Legionella makes a protective shelter. Image by herb1979 from Pixabay

Scientists have discovered how the bacteria that causes Legionnaires’ disease digs in and makes a tiny shelter inside the cells of humans and other hosts. 

The findings, published in Science, could offer insights into how other bacteria are able to survive inside cells, knowledge that could lead to new treatments for a wide variety of infections.

Discovered in 1976, Legionella, an aerobic gram-negative bacillus is responsible for Legionnaires’ disease, a condition of severe pneumonia. Spread through aerosolised water particles, it is a common cause of hospital and community-acquired pneumonia.

“Many infectious bacteria, from listeria to chlamydia to salmonella, use systems that allow them to dwell within their host’s cells,” explained study leader Vincent Tagliabracci, Ph.D., assistant professor of molecular biology at UTSW and member of the Harold C Simmons Comprehensive Cancer Center. “Better understanding the tools they use to make this happen is teaching us some interesting biochemistry and could eventually lead to new targets for therapy.”

Dr Tagliabracci’s lab studies atypical kinases, unusual forms of enzymes that put phosphates onto proteins or lipids, changing their function. Legionella is a particularly rich source of these noncanonical kinases. According to the Centers for Disease Control and Prevention, nearly 10 000 cases of Legionnaires’ disease were reported in the US in 2018, though the true incidence is believed to be higher.      

After identifying a new Legionella atypical kinase named MavQ, Dr Tagliabracci and colleagues used a live-cell imaging technique in concert with a relatively new molecular tagging method to see where MavQ is found in infected human cells. However, rather than residing in a specific location, the researchers were surprised to see that the protein moved back and forth between the endoplasmic reticulum – a network of membranes important for protein and lipid synthesis – and bubble- or tube-shaped structures within the cell.

Further research suggests that MavQ, along with a partner molecule called SidP, remodels the endoplasmic reticulum so that Legionella can strip off sections of the membrane to help create and sustain the vacuole, a structure that the parasitic bacteria uses to shelter inside cells, protecting it from immune attack.

Dr Tagliabracci said that he suspects other bacterial pathogens may use similar mechanisms to co-opt existing host cell structures to create their own protective shelters. 

 Source: University of Texas

Journal information: Ting-Sung Hsieh, et al. Dynamic remodeling of host membranes by self-organizing bacterial effectors. Science, 2021; eaay8118 DOI: 10.1126/science.aay8118

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Experimental Inhibitor Drug Shows Promise For The Deadly Marburg Virus

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Photo by CDC on Unsplash

The lethal Marburg virus, a relative of the Ebola virus, causes a serious haemorrhagic fever with an extremely high fatality rate and has had no known treatment — until now. 

Marburg virus infects human and primates, the disease currently has no approved vaccine or antivirals for prevention or treatment. In two larger recent outbreaks in the DRC in 1998–2000, and in Angola in 2004–2005, Marburg had extremely high fatality rates of 83% and 90%.

A team of researchers is working to change that. In a new paper in the journal Antimicrobial Agents and Chemotherapy, investigators from Penn’s School of Veterinary Medicine, working together with scientists from the Fox Chase Chemical Diversity Center and the Texas Biomedical Research Institute, report encouraging results from tests of an experimental antiviral targeting Marburg virus.

The new compound prevents viruses from leaving infected cells, thus halting the spread of infection. In a first, this new class of inhibitors was shown to be effective against infection in an animal model.

Additionally, possible similarities in virus-host interactions between Marburg and SARS-CoV-2, prompted the team to conducted experiments on the coronavirus. Unpublished preliminary results appeared encouraging.

“It really is exciting. These viruses are quite different but may be interacting with the same host proteins to control efficient egress and spread, so our inhibitors may be able to block them both,” said co-corresponding author Ronald Harty, Professor, Penn’s School of Veterinary Medicine.

Prof Harty’s team have been developing an antiviral that instead of targeting the virus known as “host-oriented.” By blocking the proteins in host cells that viruses hijack during late stages of infection, preventing virus-host interactions.

This method helps prevent a virus evolving resistance, but it also makes it more likely that a drug could be used against multiple viruses, as many make use of the same machinery in the host cell to reproduce and spread.

The Marburg and Ebola viruses use protein known as VP40 to interact with a host protein called Nedd4 to allow the completed viruses to ‘bud off’ of the host cell, which is a key part of viral replication.

Previously, they had tested a variety of small molecule inhibitors of this process using laboratory tests that relied on non-infectious and more-benign viral models. Those assays led them to a promising candidate, FC-10696, for further study.

The researchers firstly tested the chosen inhibitor for safety and its useful duration within the body. Next, since the real Marburg virus is too dangerous to study safely in anything but a Biosafety Level 4 (BSL-4) laboratory, they used an assay to look at what are known as virus-like particles, or VLPs, which are non-infectious but can bud off of a host cell.

Using the Biosafety Level 2 laboratory at Penn, “it’s a very quick way we can test these inhibitors,” said Prof Harty.

The researchers saw a dose-dependent response to FC-10696 on VLP budding in cells tested the compound using the real Marburg virus. These studies were done in a BSL-4 lab at Texas Biomedical Research Institute and found the compound inhibited the budding and spread of live Marburg virus in two human cell types, including in macrophages, an immune cell type commonly infected by the virus.

As a final step, they tested the compound in mice infected with Marburg virus. That received the treatment took longer to display disease symptoms and had a reduced viral load.

“These are the first promising in vivo data for our compounds,” said Prof Harty. “Whereas the control group all became sick very quickly and died, with the treated animals there was one survivor and others showed delayed onset of clinical symptoms. It’s showing that our inhibitors are having an effect.”

Source: News-Medical.Net

Journal information: Han, Z., et al. (2021) Compound FC-10696 Inhibits Egress of Marburg Virus. Antimicrobial Agents and Chemotherapy. doi.org/10.1128/AAC.00086-21.

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Night Shifts Increase Risk of Infection

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Shift working and irregular working hours can affect our health and disrupt immune response, especially in men, according to new research from the University of Waterloo.

These health-related issues occur because the body’s circadian rhythm can be disrupted by inconsistent changes in the sleep-wake schedule and feeding patterns often caused by shift work. To study this, researchers at Waterloo developed a mathematical model to investigate how a disruption in the circadian clock affects the immune system in fighting off illness.

“Because our immune system is affected by the circadian clock, our ability to mount an immune response changes during the day,” said Anita Layton, professor of Applied Mathematics, Computer Science, Pharmacy and Biology at Waterloo. “How likely are you to fight off an infection that occurs in the morning than midday? The answer depends on whether you are a man or a woman, and whether you are among [the] quarter of the modern-day labor force that has an irregular work schedule.”

The researchers created new computational models, separately for men and women, which simulate the interplay between the circadian clock and the immune system. The model is composed of the core clock genes, their related proteins, and the regulatory mechanism of pro- and anti-inflammatory mediators. By adjusting the clock, the models can simulate male and female shift-workers.

The researchers’ simulation results demonstrate that the immune response varies with the time of infection. The model simulation indicates that the time just before people go to sleep is the “worst” time to get an infection. At this point during the day, the human body is least prepared to produce the pro- and anti-inflammatory mediators needed during an infection. An individual’s sex also impacts the effect significantly.

“Shift work likely affects men and women differently,” said Stéphanie Abo, a PhD candidate in Waterloo’s Department of Applied Mathematics. “Compared to females, the immune system in males is more prone to overactivation, which can increase their chances of sepsis following an ill-timed infection.”

Source: Medical Xpress

More information: Stéphanie M. C. Abo et al. Modeling the circadian regulation of the immune system: Sexually dimorphic effects of shift work, PLOS Computational Biology (2021). DOI: 10.1371/journal.pcbi.1008514