"New research has uncovered a social world of viruses full of cheating, cooperation and other intrigues ... quantamagazine.org/viruses-finallโฆ
2) ...suggesting that viruses make sense only as members of a community."
Traditionally, viruses were thought of as solitary particles that could only replicate by infecting cells. But recent research shows viruses have complex social behaviors.
3) A new field called "sociovirology" studies the social lives of viruses, including cheating, cooperation and other interactions between viruses.
Viruses don't have social lives like humans or other species, but they do engage in social behaviors within cells and hosts.
4) Examples of viral social behaviors include competing with each other for limited resources within a cell, cooperating to evade host immune responses, and cheating by freeloading off the efforts of other viruses.
5) Sociovirology is still a young field, but its proponents believe understanding viral social lives could help explain diseases like influenza that don't make sense if viruses are viewed in isolation. It may also provide new strategies for combating viral diseases.
6) The view of viruses as solitary particles was limiting and blinded scientists to their potential complex social behaviors. This new perspective is reshape scientists' understanding of viruses and viral diseases.
7) Some viruses lack genes essential for replication. These are called "incomplete" viruses. Incomplete viruses can infect cells but cannot replicate on their own. They must "cheat" by exploiting the machinery of other viruses in the same cell.
8) If another virus with the necessary genes is present, the incomplete virus can use its polymerase to copy its own genome.
Being shorter, incomplete genomes replicate faster than complete ones when sharing resources. This gives them a sizeable advantage.
9) Other cheaters have polymerases but lack genes for protein shells. They wait to sneak their genome into shells produced by other viruses.
Researchers created "super-cheater" flu viruses that lack whole gene segments. These spread faster than normal viruses by cheating.
10) Nasal sprays of super-cheaters rapidly reduced flu in infected mice and ferrets. Surprisingly, infected ferrets also transmitted super-cheaters to others.
This raised the possibility that delivering super-cheaters to people could both cure infections and
11) ... and stop disease spread by cheating. However, human trials would be difficult due to altering viruses spread between non-consenting individuals.
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The earliest known calendar was developed in ancient Egypt around 4236 BC. It was a lunar calendar of 12 months of 30 days each. Seasons were tracked but not named.
2) Ancient civilizations first divided the year into periods based on agricultural cycles ("season" in latin means the action of sowing) and weather patterns long before formal calendars existed.
3) In all ancient civilizations, men knew that time can be divided in this interplay between environmental conditions and human action.
Likewise a seasonal disease is an infectious illness that shows a pattern of increase and decrease in incidence over the course of a year ...
2) SARS-CoV-2 can directly infect cells in the pancreas, including both exocrine and endocrine cells. It is able to infiltrate and infect pancreatic alpha, beta, delta, and pancreatic polypeptide cells.
3) In adult non-human primates (NHPs), infection causes mild pancreatic phenotypic alterations and signs of insulin resistance. Damage to the pancreas is limited.ย
In elderly NHPs, infection significantly exacerbates pancreatic pathology and damage. It causes loss of beta cells,
During viral replication, SARS-CoV-2 enters host cells through binding with ...
2) ...receptors on the cell surface. Once inside the cell, the virus releases its genetic material, which is in the form of RNA. The viral RNA then hijacks the host cell's machinery to replicate itself.
Within the Golgi apparatus, the viral RNA is translated into viral proteins..
3) ... by the host cell's ribosomes. These viral proteins undergo post-translational modifications and are processed within the Golgi apparatus. The Golgi apparatus also plays a role in assembling new viral particles.
After replication and assembly, the newly formed SARS-CoV-2 ..
2) In this first study, they evaluated the frequencies of HLA alleles in 109 Iranian COVID-19 patients and 70 healthy controls using DNA genotyping. Patients were classified as having moderate or severe disease.ย cell.com/heliyon/fullteโฆ
3) HLA-DRB1*11:01 and HLA-DRB1*04:03 were more frequent in severe patients compared to moderates, suggesting an association with increased disease severity.
HLA-DRB1*04:01 was more common in moderate patients and controls, indicating it may be protective against severe disease.
2) The SARS-CoV-2 envelope protein E is the smallest structural protein but its role in viral invasion, replication and release is not fully understood. It is known to form ion channels and alter calcium homeostasis.
3) Previous structural models of E based on NMR data showed a pentameric assembly that collapsed in simulations, without forming a stable water pore.
New molecular dynamics simulations proposed an alternative pentameric model (Model B) where helices are oriented oppositely ...
2) Post-acute sequelae of SARS-CoV-2 infection (PASC), also known as long COVID, refers to symptoms that persist beyond 12 weeks after initial infection. PASC can affect multiple organ systems including respiratory, cardiovascular, neurological, psychiatric, urinary, blood, skin
3) ...and digestive systems. Common symptoms include fatigue, headache, cough, loss of smell/taste, muscle pain.
The pathophysiology of PASC is complex and multi-factorial. Potential mechanisms include direct virus-mediated damage, immune system dysregulation/autoimmunity,