Subfamily of viruses in the family Coronaviridae

Coronaviruses are a group of related RNA viruses that cause diseases in mammals and birds. In humans, these viruses cause respiratory tract infections that can range from mild to lethal. Mild illnesses include some cases of the common cold (which is also caused by other viruses, predominantly rhinoviruses), while more lethal varieties can cause SARS, MERS, and COVID-19. Symptoms in other species vary: in chickens, they cause an upper respiratory tract disease, while in cows and pigs they cause diarrhea. There are as yet no vaccines or antiviral drugs to prevent or treat human coronavirus infections.

Coronaviruses constitute the subfamily Orthocoronavirinae, in the family Coronaviridae, order Nidovirales, and realm Riboviria.[5][6] They are enveloped viruses with a positive-sense single-stranded RNA genome and a nucleocapsid of helical symmetry.[7] The genome size of coronaviruses ranges from approximately 26 to 32 kilobases, one of the largest among RNA viruses.[8] They have characteristic club-shaped spikes that project from their surface, which in electron micrographs create an image reminiscent of the solar corona, from which their name derives.[9]

The name "coronavirus" is derived from Latin corona, meaning "crown" or "wreath", itself a borrowing from Greek korn, "garland, wreath".[10][11] The name was coined by June Almeida and David Tyrrell who first observed and studied human coronaviruses.[12] The word was first used in print in 1968 by an informal group of virologists in the journal Nature to designate the new family of viruses.[9] The name refers to the characteristic appearance of virions (the infective form of the virus) by electron microscopy, which have a fringe of large, bulbous surface projections creating an image reminiscent of the solar corona or halo.[9][12] This morphology is created by the viral spike peplomers, which are proteins on the surface of the virus.[13]

Coronaviruses were first discovered in the 1930s when an acute respiratory infection of domesticated chickens was shown to be caused by infectious bronchitis virus (IBV).[14] Arthur Schalk and M.C. Hawn described in 1931 a new respiratory infection of chickens in North Dakota. The infection of new-born chicks was characterized by gasping and listlessness. The chicks' mortality rate was 4090%.[15] Fred Beaudette and Charles Hudson six years later successfully isolated and cultivated the infectious bronchitis virus which caused the disease.[16] In the 1940s, two more animal coronaviruses, mouse hepatitis virus (MHV) and transmissible gastroenteritis virus (TGEV), were isolated.[17] It was not realized at the time that these three different viruses were related.[18]

Human coronaviruses were discovered in the 1960s.[19][20] They were isolated using two different methods in the United Kingdom and the United States.[21] E.C. Kendall, Malcom Byone, and David Tyrrell working at the Common Cold Unit of the British Medical Research Council in 1960 isolated from a boy a novel common cold virus B814.[22][23][24] The virus was not able to be cultivated using standard techniques which had successfully cultivated rhinoviruses, adenoviruses and other known common cold viruses. In 1965, Tyrrell and Byone successfully cultivated the novel virus by serially passing it through organ culture of human embryonic trachea.[25] The new cultivating method was introduced to the lab by Bertil Hoorn.[26] The isolated virus when intranasally inoculated into volunteers caused a cold and was inactivated by ether which indicated it had a lipid envelope.[22][27] Around the same time, Dorothy Hamre[28] and John Procknow at the University of Chicago isolated a novel cold virus 229E from medical students, which they grew in kidney tissue culture. The novel virus 229E, like the virus strain B814, when inoculated into volunteers caused a cold and was inactivated by ether.[29]

The two novel strains B814 and 229E were subsequently imaged by electron microscopy in 1967 by Scottish virologist June Almeida at St. Thomas Hospital in London.[30][31] Almeida through electron microscopy was able to show that B814 and 229E were morphologically related by their distinctive club-like spikes. Not only were they related with each other, but they were morphologically related to infectious bronchitis virus (IBV).[32] A research group at the National Institute of Health the same year was able to isolate another member of this new group of viruses using organ culture and named the virus strain OC43 (OC for organ culture).[33] Like B814, 229E, and IBV, the novel cold virus OC43 had distinctive club-like spikes when observed with the electron microscope.[34][35]

The IBV-like novel cold viruses were soon shown to be also morphologically related to the mouse hepatitis virus.[17] This new group of IBV-like viruses came to be known as coronaviruses after their distinctive morphological appearance.[9] Human coronavirus 229E and human coronavirus OC43 continued to be studied in subsequent decades.[36][37] The coronavirus strain B814 was lost. It is not known which present human coronavirus it was.[38] Other human coronaviruses have since been identified, including SARS-CoV in 2003, HCoV NL63 in 2004, HCoV HKU1 in 2005, MERS-CoV in 2012, and SARS-CoV-2 in 2019.[39][40] There have also been a large number of animal coronaviruses identified since the 1960s.[5]

Coronaviruses are large, roughly spherical, particles with bulbous surface projections.[41] The average diameter of the virus particles is around 125nm (.125 m). The diameter of the envelope is 85 nm and the spikes are 20nm long. The envelope of the virus in electron micrographs appears as a distinct pair of electron-dense shells (shells that are relatively opaque to the electron beam used to scan the virus particle).[42][43]

The viral envelope consists of a lipid bilayer, in which the membrane (M), envelope (E) and spike (S) structural proteins are anchored.[44] The ratio of E:S:M in the lipid bilayer is approximately 1:20:300.[45] On average a coronavirus particle has 74 surface spikes.[46] A subset of coronaviruses (specifically the members of betacoronavirus subgroup A) also have a shorter spike-like surface protein called hemagglutinin esterase (HE).[5]

The coronavirus surface spikes are homotrimers of the Sprotein, which is composed of an S1 and S2 subunit. The homotrimeric Sprotein is a class I fusion protein which mediates the receptor binding and membrane fusion between the virus and host cell. The S1 subunit forms the head of the spike and has the receptor binding domain (RBD). The S2 subunit forms the stem which anchors the spike in the viral envelope and on protease activation enables fusion. The E and M protein are important in forming the viral envelope and maintaining its structural shape.[43]

Inside the envelope, there is the nucleocapsid, which is formed from multiple copies of the nucleocapsid (N) protein, which are bound to the positive-sense single-stranded RNA genome in a continuous beads-on-a-string type conformation.[43][47] The lipid bilayer envelope, membrane proteins, and nucleocapsid protect the virus when it is outside the host cell.[48]

Coronaviruses contain a positive-sense, single-stranded RNA genome. The genome size for coronaviruses ranges from 26.4 to 31.7 kilobases.[8] The genome size is one of the largest among RNA viruses. The genome has a 5 methylated cap and a 3 polyadenylated tail.[43]

The genome organization for a coronavirus is 5-leader-UTR-replicase (ORF1ab)-spike (S)-envelope (E)-membrane (M)-nucleocapsid (N)-3UTR-poly (A) tail. The open reading frames 1a and 1b, which occupy the first two-thirds of the genome, encode the replicase polyprotein (pp1ab). The replicase polyprotein self cleaves to form 16 nonstructural proteins (nsp1nsp16).[43]

The later reading frames encode the four major structural proteins: spike, envelope, membrane, and nucleocapsid.[49] Interspersed between these reading frames are the reading frames for the accessory proteins. The number of accessory proteins and their function is unique depending on the specific coronavirus.[43]

Infection begins when the viral spike protein attaches to its complementary host cell receptor. After attachment, a protease of the host cell cleaves and activates the receptor-attached spike protein. Depending on the host cell protease available, cleavage and activation allows the virus to enter the host cell by endocytosis or direct fusion of the viral envelop with the host membrane.[50]

On entry into the host cell, the virus particle is uncoated, and its genome enters the cell cytoplasm. The coronavirus RNA genome has a 5 methylated cap and a 3 polyadenylated tail, which allows it to act like a messenger RNA and be directly translated by the host cell's ribosomes. The host ribosomes translate the initial overlapping open reading frames ORF1a and ORF1b of the virus genome into two large overlapping polyproteins, pp1a and pp1ab.[43]

The larger polyprotein pp1ab is a result of a -1 ribosomal frameshift caused by a slippery sequence (UUUAAAC) and a downstream RNA pseudoknot at the end of open reading frame ORF1a.[51] The ribosomal frameshift allows for the continuous translation of ORF1a followed by ORF1b.[43]

The polyproteins have their own proteases, PLpro (nsp3) and 3CLpro (nsp5), which cleave the polyproteins at different specific sites. The cleavage of polyprotein pp1ab yields 16 nonstructural proteins (nsp1 to nsp16). Product proteins include various replication proteins such as RNA-dependent RNA polymerase (nsp12), RNA helicase (nsp13), and exoribonuclease (nsp14).[43]

A number of the nonstructural proteins coalesce to form a multi-protein replicase-transcriptase complex. The main replicase-transcriptase protein is the RNA-dependent RNA polymerase (RdRp). It is directly involved in the replication and transcription of RNA from an RNA strand. The other nonstructural proteins in the complex assist in the replication and transcription process. The exoribonuclease nonstructural protein, for instance, provides extra fidelity to replication by providing a proofreading function which the RNA-dependent RNA polymerase lacks.[52]

Replication One of the main functions of the complex is to replicate the viral genome. RdRp directly mediates the synthesis of negative-sense genomic RNA from the positive-sense genomic RNA. This is followed by the replication of positive-sense genomic RNA from the negative-sense genomic RNA.[43]

Transcription The other important function of the complex is to transcribe the viral genome. RdRp directly mediates the synthesis of negative-sense subgenomic RNA molecules from the positive-sense genomic RNA. This process is followed by the transcription of these negative-sense subgenomic RNA molecules to their corresponding positive-sense mRNAs.[43] The subgenomic mRNAs form a "nested set" which have a common 5'-head and partially duplicate 3'-end.[53]

Recombination The replicase-transcriptase complex is also capable of genetic recombination when at least two viral genomes are present in the same infected cell.[53] RNA recombination appears to be a major driving force in determining genetic variability within a coronavirus species, the capability of a coronavirus species to jump from one host to another and, infrequently, in determining the emergence of novel coronaviruses.[54] The exact mechanism of recombination in coronaviruses is unclear, but likely involves template switching during genome replication.[54]

The replicated positive-sense genomic RNA becomes the genome of the progeny viruses. The mRNAs are gene transcripts of the last third of the virus genome after the initial overlapping reading frame. These mRNAs are translated by the host's ribosomes into the structural proteins and a number of accessory proteins.[43] RNA translation occurs inside the endoplasmic reticulum. The viral structural proteins S, E, and M move along the secretory pathway into the Golgi intermediate compartment. There, the Mproteins direct most protein-protein interactions required for assembly of viruses following its binding to the nucleocapsid. Progeny viruses are then released from the host cell by exocytosis through secretory vesicles. Once released the viruses can infect other host cells.[55]

Infected carriers are able to shed viruses into the environment. The interaction of the coronavirus spike protein with its complementary cell receptor is central in determining the tissue tropism, infectivity, and species range of the released virus.[56][57] Coronaviruses mainly target epithelial cells.[5] They are transmitted from one host to another host, depending on the coronavirus species, by either an aerosol, fomite, or fecal-oral route.[58]

Human coronaviruses infect the epithelial cells of the respiratory tract, while animal coronaviruses generally infect the epithelial cells of the digestive tract.[5] SARS coronavirus, for example, infects via an aerosol route,[59] the human epithelial cells of the lungs by binding to the angiotensin-converting enzyme 2 (ACE2) receptor.[60] Transmissible gastroenteritis coronavirus (TGEV) infects, via a fecal-oral route,[58] the pig epithelial cells of the digestive tract by binding to the alanine aminopeptidase (APN) receptor.[43]

The scientific name for coronavirus is Orthocoronavirinae or Coronavirinae.[2][3][4] Coronaviruses belong to the family of Coronaviridae, order Nidovirales, and realm Riboviria.[5][6] They are divided into alphacoronaviruses and betacoronaviruses which infect mammals and gammacoronaviruses and deltacoronaviruses, which primarily infect birds.[61][62]

The most recent common ancestor (MRCA) of all coronaviruses is estimated to have existed as recently as 8000 BCE, although some models place the common ancestor as far back as 55 million years or more, implying long term coevolution with bat and avian species.[63] The most recent common ancestor of the alphacoronavirus line has been placed at about 2400 BCE, of the betacoronavirus line at 3300 BCE, of the gammacoronavirus line at 2800 BCE, and of the deltacoronavirus line at about 3000 BCE. Bats and birds, as warm-blooded flying vertebrates, are an ideal natural reservoir for the coronavirus gene pool (with bats the reservoir for alphacoronaviruses and betacoronavirus and birds the reservoir for gammacoronaviruses and deltacoronaviruses). The large number and global range of bat and avian species that host viruses has enabled extensive evolution and dissemination of coronaviruses.[64]

Many human coronaviruses have their origin in bats.[65] The human coronavirus NL63 shared a common ancestor with a bat coronavirus (ARCoV.2) between 1190 and 1449 CE.[66] The human coronavirus 229E shared a common ancestor with a bat coronavirus (GhanaGrp1 Bt CoV) between 1686 and 1800 CE.[67] More recently, alpaca coronavirus and human coronavirus 229E diverged sometime before 1960.[68] MERS-CoV emerged in humans from bats through the intermediate host of camels.[69] MERS-CoV, although related to several bat coronavirus species, appears to have diverged from these several centuries ago.[70] The most closely related bat coronavirus and SARS-CoV diverged in 1986.[71] A possible path of evolution of SARS coronavirus and keen bat coronaviruses is that SARS-related coronaviruses coevolved in bats for a long time. The ancestors of SARS-CoV first infected leaf-nose bats of the genus Hipposideridae; subsequently, they spread to horseshoe bats in the species Rhinolophidae, then to Asian palm civets, and finally to humans.[72][73]

Unlike other betacoronaviruses, bovine coronavirus of the species Betacoronavirus 1 and subgenus Embecovirus is thought to have originated in rodents and not in bats.[65][74] In the 1790s, equine coronavirus diverged from the bovine coronavirus after a cross-species jump.[75] Later in the 1890s, human coronavirus OC43 diverged from bovine coronavirus after another cross-species spillover event.[76][75] It is speculated that the flu pandemic of 1890 may have been caused by this spillover event, and not by the influenza virus, because of the related timing, neurological symptoms, and unknown causative agent of the pandemic.[77] Besides causing respiratory infections, human coronavirus OC43 is also suspected of playing a role in neurological diseases.[78] In the 1950s, the human coronavirus OC43 began to diverge into its present genotypes.[79] Phylogentically, mouse hepatitis virus (Murine coronavirus), which infects the mouse's liver and central nervous system,[80] is related to human coronavirus OC43 and bovine coronavirus. Human coronavirus HKU1, like the aforementioned viruses, also has its origins in rodents.[65]

Coronaviruses vary significantly in risk factor. Some can kill more than 30% of those infected, such as MERS-CoV, and some are relatively harmless, such as the common cold.[43] Coronaviruses can cause colds with major symptoms, such as fever, and a sore throat from swollen adenoids.[81] Coronaviruses can cause pneumonia (either direct viral pneumonia or secondary bacterial pneumonia) and bronchitis (either direct viral bronchitis or secondary bacterial bronchitis).[82] The human coronavirus discovered in 2003, SARS-CoV, which causes severe acute respiratory syndrome (SARS), has a unique pathogenesis because it causes both upper and lower respiratory tract infections.[82]

Six species of human coronaviruses are known, with one species subdivided into two different strains, making seven strains of human coronaviruses altogether.

Four human coronaviruses produce symptoms that are generally mild:

Three human coronaviruses produce symptoms that are potentially severe:

The human coronaviruses HCoV-OC43, HCoV-HKU1, HCoV-229E, and HCoV-NL63 continually circulate in the human population and produce the generally mild symptoms of the common cold in adults and children worldwide.[83] These coronaviruses cause about 15% of common colds,[84] while 40 to 50% of colds are caused by rhinoviruses.[85] The four mild coronaviruses have a seasonal incidence occurring in the winter months in temperate climates.[86][87] There is no preponderance in any season in tropical climates.[88]

In 2003, following the outbreak of severe acute respiratory syndrome (SARS) which had begun the prior year in Asia, and secondary cases elsewhere in the world, the World Health Organization (WHO) issued a press release stating that a novel coronavirus identified by a number of laboratories was the causative agent for SARS. The virus was officially named the SARS coronavirus (SARS-CoV). More than 8,000 people were infected, about ten percent of whom died.[60]

In September 2012, a new type of coronavirus was identified, initially called Novel Coronavirus 2012, and now officially named Middle East respiratory syndrome coronavirus (MERS-CoV).[98][99] The World Health Organization issued a global alert soon after.[100] The WHO update on 28 September 2012 said the virus did not seem to pass easily from person to person.[101] However, on 12 May 2013, a case of human-to-human transmission in France was confirmed by the French Ministry of Social Affairs and Health.[102] In addition, cases of human-to-human transmission were reported by the Ministry of Health in Tunisia. Two confirmed cases involved people who seemed to have caught the disease from their late father, who became ill after a visit to Qatar and Saudi Arabia. Despite this, it appears the virus had trouble spreading from human to human, as most individuals who are infected do not transmit the virus.[103] By 30 October 2013, there were 124 cases and 52 deaths in Saudi Arabia.[104]

After the Dutch Erasmus Medical Centre sequenced the virus, the virus was given a new name, Human CoronavirusErasmus Medical Centre (HCoV-EMC). The final name for the virus is Middle East respiratory syndrome coronavirus (MERS-CoV). The only U.S. cases (both survived) were recorded in May 2014.[105]

In May 2015, an outbreak of MERS-CoV occurred in the Republic of Korea, when a man who had traveled to the Middle East, visited four hospitals in the Seoul area to treat his illness. This caused one of the largest outbreaks of MERS-CoV outside the Middle East.[106] As of December 2019, 2,468 cases of MERS-CoV infection had been confirmed by laboratory tests, 851 of which were fatal, a mortality rate of approximately 34.5%.[107]

In December 2019, a pneumonia outbreak was reported in Wuhan, China.[108] On 31 December 2019, the outbreak was traced to a novel strain of coronavirus,[109] which was given the interim name 2019-nCoV by the World Health Organization (WHO),[110][111][112] later renamed SARS-CoV-2 by the International Committee on Taxonomy of Viruses.

As of 14 July 2020, there have been at least 572,411[94] confirmed deaths and more than 13,070,097[94] confirmed cases in the COVID-19 pandemic. The Wuhan strain has been identified as a new strain of Betacoronavirus from group 2B with approximately 70% genetic similarity to the SARS-CoV.[113] The virus has a 96% similarity to a bat coronavirus, so it is widely suspected to originate from bats as well.[114][115] The pandemic has resulted in travel restrictions and nationwide lockdowns in many countries.

Coronaviruses have been recognized as causing pathological conditions in veterinary medicine since the 1930s.[17] They infect a range of animals including swine, cattle, horses, camels, cats, dogs, rodents, birds and bats.[116] The majority of animal related coronaviruses infect the intestinal tract and are transmitted by a fecal-oral route.[117] Significant research efforts have been focused on elucidating the viral pathogenesis of these animal coronaviruses, especially by virologists interested in veterinary and zoonotic diseases.[118]

Coronaviruses infect domesticated birds.[119] Infectious bronchitis virus (IBV), a type of coronavirus, causes avian infectious bronchitis.[120] The virus is of concern to the poultry industry because of the high mortality from infection, its rapid spread, and its effect on production.[116] The virus affects both meat production and egg production and causes substantial economic loss.[121] In chickens, infectious bronchitis virus targets not only the respiratory tract but also the urogenital tract. The virus can spread to different organs throughout the chicken.[120] The virus is transmitted by aersol and food contaminated by feces. Different vaccines against IBV exist and have helped to limit the spread of the virus and its variants.[116] Infectious bronchitis virus is one of a number of strains of the species Avian coronavirus.[122] Another strain of avian coronavirus is turkey coronavirus (TCV) which causes enteritis in turkeys.[116]

Coronaviruses also affect other branches of animal husbandry such as pig farming and the cattle raising.[116] Swine acute diarrhea syndrome coronavirus (SADS-CoV), which is related to bat coronavirus HKU2, causes diarrhea in pigs.[123] Porcine epidemic diarrhea virus (PEDV) is a coronavirus that has recently emerged and similarly causes diarrhea in pigs.[124] Transmissible gastroenteritis virus (TGEV), which is a member of the species Alphacoronavirus 1,[125] is another coronavirus that causes diarrhea in young pigs.[126][127] In the cattle industry bovine coronavirus (BCV), which is a member of the species Betacoronavirus 1 and related to HCoV-OC43,[128] is responsible for severe profuse enteritis in young calves.[116]

Coronaviruses infect domestic pets such as cats, dogs, and ferrets.[119] There are two forms of feline coronavirus which are both members of the species Alphacoronavirus 1.[125] Feline enteric coronavirus is a pathogen of minor clinical significance, but spontaneous mutation of this virus can result in feline infectious peritonitis (FIP), a disease with high mortality.[116] There are two different coronaviruses that infect dogs. Canine coronavirus (CCoV), which is a member of the species Alphacoronavirus 1,[125] causes mild gastrointestinal disease.[116] Canine respiratory coronavirus (CRCoV), which is a member of the species Betacoronavirus 1 and related to HCoV-OC43,[128] cause respiratory disease.[116] Similarly, there are two types of coronavirus that infect ferrets.[129] Ferret enteric coronavirus causes a gastrointestinal syndrome known as epizootic catarrhal enteritis (ECE), and a more lethal systemic version of the virus (like FIP in cats) known as ferret systemic coronavirus (FSC).[130][131]

Coronaviruses infect laboratory animals.[116] Mouse hepatitis virus (MHV), which is a member of the species Murine coronavirus,[132] causes an epidemic murine illness with high mortality, especially among colonies of laboratory mice.[133] Prior to the discovery of SARS-CoV, MHV was the best-studied coronavirus both in vivo and in vitro as well as at the molecular level. Some strains of MHV cause a progressive demyelinating encephalitis in mice which has been used as a murine model for multiple sclerosis.[118] Sialodacryoadenitis virus (SDAV), which is a strain of the species Murine coronavirus,[132] is highly infectious coronavirus of laboratory rats, which can be transmitted between individuals by direct contact and indirectly by aerosol. Acute infections have high morbidity and tropism for the salivary, lachrymal and harderian glands.[134] Rabbit enteric coronavirus causes acute gastrointestinal disease and diarrhea in young European rabbits.[116] Mortality rates are high.[135]

There are no vaccines or antiviral drugs to prevent or treat human coronavirus infections. Treatment is only supportive. A number of antivirial targets have been identified such as viral proteases, polymerases, and entry proteins. Drugs are in development which target these proteins and the different steps of viral replication. A number of vaccines using different methods are also under development for different human coronaviruses.[43]

There are no antiviral drugs to treat animal coronaviruses.[citation needed] Vaccines are available for IBV, TGEV, and Canine CoV, although their effectiveness is limited. In the case of outbreaks of highly contagious animal coronaviruses, such as PEDV, measures such as destruction of entire herds of pigs may be used to prevent transmission to other herds.[43]

Originally posted here:

Coronavirus - Wikipedia

The evidence that this type of transmission is happening with SARS-CoV-2arguably already exists.Several big studiespoint to airborne transmission of the virus as a major routefor the spread of covid-19. Other studies have suggested the virus can remain in aerosolized droplets for hours. One new study led by Roy and his team at Tulane shows that infectious aerosolized particles of SARS-CoV-2 could actually linger in the air for up to 16 hours, and maintain infectivity much longer than MERS and SARS-CoV-1 (the other big coronaviruses to emerge this century).

We still dont know what gives SARS-CoV-2 this airborne edge. But it may be one reason this is a pandemic, and not simply a small outbreak like any other coronavirus, says Roy.

Whether the virus is airborne isnt simply a scientific question. If it is, it could mean that in places where the virus has not been properly contained (e.g., the US), the economy needs to be reopened more slowly, under tighter regulations that reinforce current health practices as well as introducing improved ones. Our current tactics for stopping the spread wont be enough.

Roy would like to see aggressive mandates on strict mask use for anyone leaving home. This virus sheds like crazy, he says. Masking can do an incredible amount in breaking transmission. I think anything that can promote the use of masking, to stop the production of aerosols in the environment, would be helpful.

Brosseau, however, says that though masks can limit the spread of larger particles, they are less helpful for smaller ones, especially if they fit only loosely. I wish we would stop relying on the idea that face coverings are going to solve everything and help flatten the curve, she says. Its magical thinkingits not going to happen. For masks to really make a difference, they would need to be worn all the time, even around family.

Brosseau does believe the evidence is trending toward the conclusion that airborne transmission is the primary and possibly most important mode of transmission for SARS-CoV-2. She says, I think the amount of time and effort devoted to sanitizing every single surface over and over and over again has been a huge waste of time. We dont need to worry so much about cleaning every single surface we touch. Instead, the focus should be on other factors, like where we spend our time.

One of the biggest questions we still have about covid-19 is how much of a viral load is needed to cause infection. The answer changes if we think it is aerosols that we need to worry about. Smaller particles wont carry as large a viral load as bigger ones, but because they can linger in the air for much longer, it may not mattertheyll build up in larger concentrations and get distributed more widely the longer an infected person is around to expel aerosolized virus.

The more people you have coming in and out of an indoor space, the more likely it is that someone who is infected will show up. The longer those infected individuals spend in that space, the higher the concentration of virus in the air over time. This is particularly bad news for spaces where people congregate for hours on end, like restaurants, bars, offices, classrooms, and churches.

Airborne transmission doesnt necessarily mean these places must stay closed (although that would be ideal). But wiping down surfaces with disinfectant, and having everyone wear masks, wont be enough. To safely reopen, these spots will not just need to reduce the number of people allowed inside at any given moment; they will also need to reduce the amount of time those people spend there. Increasing social distancing beyond six feet would also help keep people safer.

Ventilation needs to be a higher priority too. This is going to be a big problem for older buildings that usually have worse ventilation systems, and areas with a lot of those might need to remain closed for much longer. The impact ofasymptomatic spread(transmission by people who dont feel ill) andsuperspreadersonly compounds the problem even further. Butresearchconducted by the US Department of Homeland Security has shown that in the presence of UV light, aerosolized particles of the size the Tulane researchers studied would disappear in less than a minute.A number of businesseshave begun deploying UV-armed robots to disinfect hospital rooms, shopping malls, stores, public transit stations, and more.

For many places, considerable delays in economic reopening might ultimately be the price of getting the virus under control. Otherwise the kind of thing that happened when a single open bar in Michiganled to an outbreak of more than 170 new casescould become commonplace.

Heading into the fall, "the implications are profoundbut not that hard to grasp," says Donald Milton, an aerobiology expert at the University of Maryland and one of the authors who spearheaded the letter to WHO. "We need to subsidize bars and restaurants to stay closed. We need to increase ventilation where we can and start making as widespread as possible use of air sanitation with upper-room germicidal UV and maybe far UV in those places that must be open, like elementary schools. We need to stagger hours of starting work and keep density on public transport low, or open windows. And we need to wear masks."

This post has been updated with additional comments from Donald Milton.

Original post:

If the coronavirus is really airborne, we might be fighting it the wrong way - MIT Technology Review

How dangerous is the virus?

There are three parameters to understand in order to assess the magnitude of the risk posed by this novel coronavirus:

The attack rate or transmissibility (how rapidly the disease spreads) of a virus is indicated by its reproductive number (Ro, pronounced R-nought or r-zero), which represents the average number of people to which a single infected person will transmit the virus.

WHO's estimated (on Jan. 23) Ro to be between 1.4 and 2.5. [13]

Other studies have estimated a Ro between 3.6 and 4.0, and between 2.24 to 3.58. [23].

Preliminary studies had estimated Ro to be between 1.5 and 3.5. [5][6][7]

An outbreak with a reproductive number of below 1 will gradually disappear.

For comparison, the Ro for the common flu is 1.3 and for SARS it was 2.0.

See full details: Coronavirus Fatality Rate

The novel coronavirus' case fatality rate has been estimated at around 2%, in the WHO press conference held on January 29, 2020 [16] . However, it noted that, without knowing how many were infected, it was too early to be able to put a percentage on the mortality rate figure.

A prior estimate [9] had put that number at 3%.

Fatality rate can change as a virus can mutate, according to epidemiologists.

For comparison, the case fatality rate for SARS was 10%, and for MERS 34%.

See full details: COVID-19 Coronavirus Incubation Period

Symptoms of COVID-19 may appear in as few as 2 days or as long as 14 (estimated ranges vary from 2-10 days, 2-14 days, and 10-14 days, see details), during which the virus is contagious but the patient does not display any symptom (asymptomatic transmission).

See latest findings: Age, Sex, Demographics of COVID-19 Cases and Deaths

According to early estimates by China's National Health Commission (NHC), about 80% of those who died were over the age of 60 and 75% of them hadpre-existing health conditions such as cardiovascular diseases anddiabetes.[24]

According to the WHO Situation Report no. 7 issued on Jan. 27:

A study of 138 hospitalized patients with NCIP found that the median age was 56 years (interquartile range, 42-68; range, 22-92 years) and 75 (54.3%) were men.[25]

The WHO, in its Myth busters FAQs, addresses the question: "Does the new coronavirus affect older people, or are younger people also susceptible?" by answering that:

As of Jan. 29, according to French authorities, the conditions of the two earliest Paris cases had worsened and the patients were being treated in intensive care, according to French authorities. The patients have been described as a young couple aged 30 and 31 years old, both Chinese citizens from Wuhan who were asymptomatic when they arrived in Paris on January 18 [19].

The NHC reported the details of the first 17 deaths up to 24 pm on January 22, 2020. The deaths included 13 males and 4 females. The median age of the deaths was 75 (range 48-89) years.[21]

See full details: WHO coronavirus updates

On January 30, the World Health Organization declared the coronavirus outbreak a Global Public Health Emergency.

For more information from the WHO regarding novel coronavirus: WHO page on Novel Coronavirus (2019-nCoV)

Read the rest here:

Coronavirus Update (Live): 11,845,377 Cases and 543,553 ...

Find developments on Washington's coronavirus outbreak and the state's plan for recovery.

Monday, July 13:

3% of frontline UW Medicine workers tested have COVID-19 antibodies

About 3% of frontline UW Medicine workers showed prevalence for previous COVID-19 infection during a round of recent antibody tests.

UW Medicine says this prevalence rate is lower than the general public indicating there is not a significantly higher risk of coronavirus among frontline workers versus the general population.

The first round of antibody tests focused on staff at Harborview Medical Center, UW Medical Center, Airlift Northwest and UW neighborhood clinics who have direct exposure to COVID-19 patients. UW Medicine plans to administer a second round of antibody tests to workers in regular inpatient units and a third round of tests to other staff.

Inslee requests extension of National Guard mission

Citing the coronavirus pandemic, Gov. Jay Inslee sent a letter to the Trump administration today requesting an extension of federal authority and funding for Washington National Guard employment.

The letter reads, in part:

"As the number of positive COVID-19 cases continues to climb in our state, it is clear that help from the Washington National Guard remains essential through the end of the year ... Currently, more than 1,000 Citizen-Soldiers and Airmen are assisting with critical missions that keep our food banks operational and our neighbors fed. They are critical to our efforts to slow the spread of the virus by supporting COVID-mapping missions, assembling test kits, and operating community-based test sites. Additionally, uniquely skilled National Guard planners are assisting my COVID-19 food security team and other state agencies to ensure that we meet the health and welfare needs of Washingtonians through our phased re-opening plan."

Paid parking enforcement resumes in Seattle

On-street paid parking and parking enforcement resumed in Seattle on Monday.

Paid parking and limited parking enforcement were suspended in April in response to Gov. Jay Inslee's "Stay Home, Stay Health" order.

With King County's transition to Phase 2 of the state's reopening plan and more businesses reopening, "reliable access at the curb for customers is critical for recovery," SDOT posted.

Parking will be 50 cents per hour in all areas, the minimum rate allowed according to city code. That rate will remain for at least a month while SDOT reviews data related to parking activity and occupancy in business districts.

Enforcement of free, hourly parking will resume as well.

People younger than 40 accounts for almost three-quarters of King County cases in past two weeks

King Countys top public health official says COVID-19 isnt going away soon, so people need to learn to make protecting each others health part of daily life. Dr. Jeff Duchin, health officer for Public Health - Seattle & King County, said Friday that people need to understand the long-term nature of COVID-19.

King County saw an average of 118 new cases per day during the week ending July 9. Thats nearly triple the daily average for the week ending June 9.

Duchin says people younger than 40 accounts for almost three-quarters of King County cases during the past two weeks.

New coronavirus cases, deaths reported

There were 1,438 new coronavirus cases and 14 new deaths reported Sunday in Washington.

These totals represent new cases and deaths for two days. The Washington State Department of Health did not report new cases Saturday as the system was down for maintenance.

There are now 40,656 total confirmed cases and 1,438 deaths statewide.

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Coronavirus updates: 3% of frontline UW Medicine workers tested have antibodies - KING5.com

CHICAGO Mayor Lori Lightfoot warned restaurants, bars and other spots popular among younger Chicagoans to protect patrons from coronavirus or else they risk a crackdown.

The city has seen a rise in cases of COVID-19 among people ages 18-29, which has been concerning, Lightfoot said during a Monday press conference. Officials have said the uptick is due to to a number of reasons, including the fact young people are gathering in groups and at businesses without social distancing or face coverings.

Because of that, the city is looking at where these folks congregate, Lightfoot said.

Thats why were having a lot of conversations with bars, restaurants, other places of entertainment, Lightfoot said. And if we dont see progress, were gonna take some specific steps.

But my hope, always, is to educate people into compliance. We need to make sure that we are continuing to be diligent.

RELATED: Young Adults Now Make Up Most Of Chicagos New Coronavirus Cases, Citys Health Chief Says

Lightfoot said the city is not yet at the level of shutting down such businesses but they are pushing restaurants, bars, gyms and other places where young people gather to follow the citys rules to prevent the spread of coronavirus and emphasize that patrons should take public health rules seriously.

Im not gonna take anything off the table. I dont think were at that point [of closing again] just yet, but I am deeply concerned because we are starting to see this uptick , Lightfoot said. The case rate, the daily accumulation of cases, is something Im definitely concerned about.

And were not gonna hesitate to take the steps that are necessary if we continue to see a rise in that number.

While people age 19-29 are now making up most of Chicagos new coronavirus cases, people 30-39 have also been seeing more coronavirus cases, Lightfoot said.

The uptick among young people has been seen throughout the city, but its been particularly prominent in the Lincoln Park and New City community areas, Dr. Allison Arwady, head of the Chicago Department of Public Health, said Friday.

Arwady and Lightfoot said the rise has possibly come because younger people feel invincible and arent taken precautions like wearing face coverings and practicing social distancing.

Theres been a fair bit of spread in informal settings, like people gathering for house parties or going to businesses where requirements like social distancing arent well-enforced, Arwady said.

But young people still face risks from coronavirus, Lightfoot said.

If youre young, its still coming for you, Lightfoot said

And Arwady said the city is worried young people could transmit the virus to older Chicagoans, who are at higher risk of severe complications or death from coronavirus.

At the start of July, Lightfoot vowed tocrack down on bars and other businesses that arent following rulesfor keeping people safe amid the pandemic. That came after Block Club reported on bars reopening in Wrigleyville, where large crowds of young peopledrank and gathered on the sidewalks and at some establishments without wearing masks or practicing social distancing.

Block Club Chicagos coronavirus coverage is free for all readers. Block Club is an independent, 501(c)(3), journalist-run newsroom.

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City Will Crack Down On Bars, Gyms If Rise In Coronavirus Cases Among Young Chicagoans Continues, Lightfoot Says - Block Club Chicago

As the British authorities ease confinement restrictions but continue to fear new waves of infections, they have announced that nursing home residents will be tested for the virus monthly, with staff members tested weekly.

Mr. Johnsons government also pledged 600 million pounds, or $749 million, in support of the countrys nursing homes in May, in addition to 3.2 billion $4 billion to local governments for key public services like nursing-home facilities.

After months of waiting for a steep drop in cases that never came, many local governments have started reopening their buildings. But the business of assessing properties, paying fines and running Americas cities looks little like it did before the pandemic.

In Aurora, Ill., City Hall was set to open just three days a week, with the first hour each day set aside for older residents. In Detroits partly reopened municipal center, appointments were recommended, employees were being tested for the virus and workers were no longer accepting cash payments. And in Dayton, Ohio, where City Hall had been closed since March 18, it was set to reopen this week with hand-sanitizing stations and security guards performing temperature checks.

Even with their front doors unlocked, cities were not exactly encouraging visitors. Officials in Buffalo, who also planned to reopen, said residents with a temperature over 100.4 degrees would not be allowed inside. Detroit officials planned to offer curbside service. Daytons news release announcing its reopening included an explicit suggestion to not come:

The City of Dayton is encouraging customers to continue conducting business with the city remotely and electronically, as physical distancing standards are practiced at city facilities and many employees continue to work from home, the statement said.

All four of the large U.S. airlines have agreed to terms for loans from the federal government under the March stimulus bill, the Treasury Department said Tuesday.

Delta Air Lines, United Airlines and Southwest Airlines signed letters of intent under that law, known as the CARES Act, Treasury said. Last week, the department announced that American Airlines had agreed to a five-year $4.75 billion loan.

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Coronavirus Live Updates: Testing Demand in U.S. Soars, Creating a New Crisis - The New York Times

The federal government will pay the vaccine maker Novavax $1.6 billion to expedite the development of a coronavirus vaccine. Its the largest deal to date from Operation Warp Speed, the sprawling federal effort to make coronavirus vaccines and treatments available to the American public as quickly as possible.

The deal would pay for Novavax to produce 100 million doses of its new vaccine by the beginning of next year if the vaccine is shown to be effective in clinical trials. Thats a significant bet on Novavax, a Maryland company that has never brought a product to market.

With this deal, the federal government has now invested nearly $4 billion in companies pursuing vaccines, but has provided little information about how Operation Warp Speed is spending money, which agencies the funding is coming from or how decisions are being made.

That money has gone to six companies with varying track records and, in many cases, promising but untested technologies. British drugmaker AstraZeneca has received $1.2 billion in federal assistance for its vaccine, which uses a harmless virus to provoke an immune response. Moderna Therapeutics, which has received more than $500 million, also has never brought a product to market and is using a genetic technology that is valued for its speed but has never led to a successful human vaccine.

Some say the administrations strategy backing a variety of approaches, including some that are cutting-edge but may not work is the best way to move quickly in the middle of a deadly pandemic. But critics say the public deserves to know more about how taxpayer money is being spent at this critical moment.

Its a black box, said Peter Maybarduk, the director of the global access to medicines program at Public Citizen, a public interest group. This could be one of the most important medical technologies of our time, and we know very little about how that money is being spent, and what conditions are being placed on it.

Officials have given varying estimates of how many treatments and vaccines are part of Operation Warp Speed, and have declined to give the full list of which companies are participating. Congress has appropriated nearly $10 billion to support development of a coronavirus treatment or vaccine, but Trump administration officials have said that billions more could ultimately be spent, without providing additional details. A flurry of contracts with vaccine and drug manufacturers were recently made public, but the documents were heavily redacted and provided little information about the arrangements with the companies.

Operation Warp Speed leaders analyze all possible therapeutics and vaccine partners, select the most promising candidates, and then follow standard protocol on contract awards and spending, said Michael Caputo, assistant secretary for public affairs at the department of health and human services. While these experts are moving quickly and focused on safety, were putting a lot of effort into assuring transparency while not tangling them up in constant media inquiries.

In an interview on Sunday, Novavaxs president and chief executive, Stanley C. Erck, initially said he was not sure where in the government the $1.6 billion was coming from. A Novavax spokeswoman later said the money was coming from a collaboration between the Health and Human Services Department and the Defense Department.

Adding Novavaxs candidate to Operation Warp Speeds diverse portfolio of vaccines increases the odds that we will have a safe, effective vaccine as soon as the end of this year, Alex M. Azar II, the health and human services secretary, said in a statement.

Until now, new vaccines have taken years to develop, and many vaccines fail in clinical trials when they turn out to be ineffective or to cause serious side effects. Many experts have said the aggressive timelines set by companies and government officials for a coronavirus vaccine are overly optimistic.

Mr. Erck said Novavaxs coronavirus vaccine uses the same technology as its other experimental vaccines, such as one for the flu, that have been tested in late-stage clinical trials. Novavax has recently brought in senior executives from established manufacturers like AstraZeneca and GlaxoSmithKline, he said.

The risk theyre taking is that a company like ours which doesnt have a pipeline of already commercialized products can we get to the big leagues and scale up? he said. And I think theyre placing the bet that we can.

The U.S. investment comes after an international group, the Coalition for Epidemic Preparedness Innovations, awarded up to $388 million to Novavax in May to make its coronavirus vaccine available globally.

Several vaccine experts said Novavaxs vaccine would help diversify the federal portfolio by including another candidate that uses a protein-based vaccine that has worked against other pathogens, like hepatitis B. The Novavax vaccine uses microscopic particles that carry fragments of the coronavirus, prompting the bodys immune system to respond. Sanofi, which has received nearly $31 million in government funding, is also developing a vaccine that is based on viral proteins.

This is a sort of diversification from other approaches, which makes a certain amount of sense, said John P. Moore, a professor of microbiology and immunology at Weill Cornell Medical College in New York City. You dont want all of your eggs in one basket.

Mr. Erck said the deal with the United States would allow Novavax to begin manufacturing the vaccines before the company concludes late-stage clinical trials, expected by the end of the year. The company would ensure that 100 million doses enough for 50 million people to receive an initial shot and a booster are delivered by the first quarter of 2021, if its coronavirus vaccine is proved safe and effective. In June, Novavax secured a $60 million contract from the Defense Department to guarantee the delivery of 10 million doses to vaccinate American troops for the coronavirus.

Novavax began early-stage safety trials in Australia in May, and the company has said it expects to make the results available this month. It said it planned to begin so-called Phase 3 efficacy trials by the fall of this year and could release interim data by the end of 2020.

Through its deal with the Coalition for Epidemic Preparedness Innovations, Novavax is also setting up manufacturing in other sites around the world, including in Europe and Asia, to serve populations outside the United States. The company is using its own facilities to scale up manufacturing and will also contract with outside companies, Mr. Erck said.

He and others have noted that more than one vaccine will need to succeed in order to vaccinate the entire world. Right now, we need and want everybodys to work, he said.

Noah Weiland contributed reporting.

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Novavax Gets $1.6 Billion for Coronavirus Vaccine From Operation Warp Speed - The New York Times