Modeling coronavirus spread, or why are there different numbers of expected deaths?

[TheLurch]

The evidence is conclusive that colds, flus, MERS, SARS, numerous other viruses, and COVAG 19 are of course, all viruses, but that is where similarity ends.

No, that's absolutely and unequivocally wrong. Viruses have the same phylogeny that living organisms do (class, order, family, etc.). Flu viruses are very distantly related to coronaviruses. Colds are caused by multiple, unrelated viruses. All coronaviruses belong to one of two closely related genera, which means there is extensive similarity among them in terms of gene content, genome organization, etc. Thus, MERS is very similar to both instances of SARS, unlike the other viruses you mention.

You're as bad as Lee about making statements that have no basis in biology.

[shunyadragon]

No, that's absolutely and unequivocally wrong. Viruses have the same phylogeny that living organisms do (class, order, family, etc.). Flu viruses are very distantly related to coronaviruses. Colds are caused by multiple, unrelated viruses. All coronaviruses belong to one of two closely related genera, which means there is extensive similarity among them in terms of gene content, genome organization, etc. Thus, MERS is very similar to both instances of SARS, unlike the other viruses you mention.

You're as bad as Lee about making statements that have no basis in biology.

I n this case I consider you as bad at biology as Lee. What is your agenda. There are definitely regional differences in the viruses and their relationship with the hosts.

I made no statements as you indicate concerning flus, and colds except that they are more universal than other regional viruses like MERS in the Middle East, and SARS and COVAG 19 in China.

[shunyadragon]

Why not?

. . . because you do not acknowledge the documented history of the differences in the regional viruses and their relationship with the hosts, and the herd immunity.

[TheLurch]

What is your agenda.

My agenda is to provide accurate scientific information. Therefore, when someone says that the similarity between MERS and SARS ends with "they're viruses", i'll correct that.

[shunyadragon]

My agenda is to provide accurate scientific information. Therefore, when someone says that the similarity between MERS and SARS ends with "they're viruses", i'll correct that.

All viruses are similar. So What?!?!!? The sky is Carolina blue on a clear day at noon too. That is not the question at hand which you are dodging.

. . . because you do not acknowledge the documented history of the differences in the regional viruses and their relationship with the hosts, and the herd immunity.

I am waiting for more research on the genetics of the viruses and believe similar strains have been back and forth from animals to humans for some time as less virulent strains before it became the virus causing a pandemic.

[TheLurch]

And of course it's the more important link.



But it's also the same link I shared earlier.

As far as I can tell, your summary of the Imperial College paper is accurate. What level students are you teaching it to?

[TheLurch]

All viruses are similar. So What?!?!!? The sky is Carolina blue on a clear day at noon too. That is not the question at hand which you are dodging.

Why don't you compare the herpes virus genome to that of MERS and SARS and get back to me on that statement?

[shunyadragon]

Why don't you compare the herpes virus genome to that of MERS and SARS and get back to me on that statement?

I am not sure where the comparison goes, but I will look at herpes nonetheless. The genome may be similar, which is likely where you are going, but I would interested in the regional history of the herpes virus also. The only comment right now from memory is it is a global virus with regional variations maybe,

[Juvenal]

As far as I can tell, your summary of the Imperial College paper is accurate. What level students are you teaching it to?

Undergrads from Trig to Calc 2 this term, meaning they'd all been exposed to exponential functions even if they never recovered. And thanks! We took a two week break to gear up for "remote learning," resuming classes on 3/30, two days after my analysis was posted here.

By that time I'd also derived a formula for herd immunity, 1 - 1/R0 ...

2020-04-12_01-13-32.jpg

... which doesn't seem to appear in any news articles, but goes a long way toward explaining how optimal mitigation could cut the fatalities in half by preventing significant overshoot of herd immunity and by weighting infections toward less vulnerable age groups.

Of course, that's not "optimal" optimal for mitigation.

There's the Dr. Strangelove plan ... round up everyone under 45 and invite them to a covid-19 party ... herd immunity at the cost of just 80,000 deaths.

Dr Strangelove.jpg

[TheLurch]

I am not sure where the comparison goes, but I will look at herpes nonetheless. The genome may be similar, which is likely where you are going, but I would interested in the regional history of the herpes virus also. The only comment right now from memory is it is a global virus with regional variations maybe,

The point is for you to realize that saying "All viruses are similar" is simply wrong.

[shunyadragon]

The point is for you to realize that saying "All viruses are similar" is simply wrong.

No, that is not the point, yes all viruses are similar so what, all rodents are similar. I believe there is significant regional differences among the some' herpes virus.

[shunyadragon]

Why don't you compare the herpes virus genome to that of MERS and SARS and get back to me on that statement?

Actually thank you for inspiring me to search this, because the following reference provides some insight into the 'possible' coevolution of virus and host.

Source: https://jvi.asm.org/content/88/2/1209

Comments on HSV-1 evolution. This paper presents the first survey of HSV-1 variation that has near-global coverage and incorporates both coding and noncoding features of the genome. Geographical clustering prevails despite signs of recombination (Fig. 8 and 9). During the coevolution of humans and HSV-1, spatial segregation of ancestral host populations is likely to have generated some geographic isolation of viral lineages. Similar impacts of geographic separation on the results of viral genome clustering have been observed for VZV (12, 15, 155, 156). The current study, in combination with prior work, indicates extensive recombination between HSV-1 genomes (Fig. 9), at a level that far exceeds that observed for VZV (13, 15, 156). While dating of VZV evolution has been proposed based on similar data, we find that the prevalence of recombination in HSV-1 makes it unwise to add a time scale to internal nodes or to interpret these clusters as clades (13, 155, 157).

Although past geographical separation may well have impacted the currently available sequences, it is worth noting that all of the currently sequenced genomes were isolated more than 25 years ago (Table 1). The degree and extent of human global movement and interaction have increased at a pace that begs future projects to encompass currently circulating strains. Progress in VZV genome sequencing and comparison has moved more rapidly in this regard (158, 159). It has been proposed that the geographically linked clade structure of VZV may be fading under the impact of host mixing (12, 155, 160), whereas the signs of recombination suggest that even decades ago, when these strains were collected, HSV-1 strains were already a single, panmictic population (Fig. 8). Future sequencing efforts will be needed to assess whether the rate of mixing among HSV strains has increased due to human movement and to assess the modern extent of HSV-1 interstrain diversity as a result. These data will be crucial to our understanding of the efficacy of vaccine candidates and to the development of widely effective therapeutics.

The preponderant mode of protein evolution appears to be moderate constraint, although the outliers range from tight constraint to near neutrality (Fig. 6). We found evidence for a few residues being under positive selection using stringent tests (Table 3; see also Table S4 in the supplemental material), and borderline signals were obtained for many more residues. As further sequences become available, more extensive sampling of protein variability will provide a clearer picture of selective pressures. Likewise, testing of the alternative versions of positively selected residues, such as those found in gH (UL22) and UL42 (Fig. 7), will determine their relative efficacies and how these variations affect viral spread between hosts.

These data present a rich resource for mining information about the coevolution of HSV and the human immune response, which will in turn be relevant for the development of highly stimulatory vaccine antigens. For instance, gB (UL27) has been a key vaccine target in several recent trials (5). These data reveal that more than half of the variation among HSV strains in this 904-amino-acid protein occurs in the first 80 residues (see Table S3 in the supplemental material; see also reference 161). This N-terminal fragment lies outside the gB crystal structure (162). The functions of this region are not well defined but include a binding site for major histocompatibility complex (MHC) class II molecules (163). Some of the most variable gB residues (residues 59 to 80, of which one-third are variable) are also highly antigenic and capable of stimulating immunity (164, 165). Knowledge of interstrain variations in gB and other viral proteins will allow the refinement of vaccine antigens to create a strong and broadly effective immune response.

As future studies add to our knowledge of HSV genome diversity, it will be important to maintain as much clinical and passage history data as possible. The current sequences reveal a wealth of data about genetic diversity among HSV-1 strains, but we now need to enrich these data by capturing information about specific strain origins, disease presentation, immune status, passage history for cultured strains, and related metadata. Community-wide resources, such as GenBank and the Virus Pathogen Resource, provide avenues to include these data alongside newly produced sequences (69). These approaches will aid future analyses of genetic links to phenotype, host status, and disease progression.

ACKNOWLEDGMENTS
We are grateful for the tremendous contributions of two retired colleagues: Hiroshi Sakaoka, who characterized hundreds of HSV-1 strains during his career, and Duncan McGeoch, who sequenced the first HSV-1 genome and provided the driving force to sequence the collection described here. We thank Lance Parsons for feedback on analyses and construction of the website at http://szparalab.psu.edu/hsv-diversity/. Yolanda Tafuri assisted in strain propagation, and Derrick Dargan, Clare Addison, and Tracey Neilson recovered HSV-1 strains by transfection. High-throughput sequencing was carried out at the Sir Henry Wellcome Functional Genomics Facility (University of Glasgow), the Gene Pool (University of Edinburgh), and the High-Throughput Genomics Group at the Wellcome Trust Centre for Human Genetics (University of Oxford).

This work was supported by the NIH-NIAID Virus Pathogen Resource (ViPR) Bioinformatics Resource Center (BRC), NIH-NIGMS Center (grant P50 GM071508), and NIH (grant P40 RR 018604 [M.L.S. and L.W.E.]), by the UK Medical Research Council (A.J.D., D.G., and A.D.), by the Eric and Wendy Schmidt Member in Biology fund (B.G.), and by the Wellcome Trust (grant 090532/Z/09/Z) and MRC Hub (grant G0900747 91070 [R.J.B.]).

© Copyright Original Source

[TheLurch]

No, that is not the point, yes all viruses are similar so what, all rodents are similar. I believe there is significant regional differences among the some' herpes virus.

Unreal. You do realize that viruses can store their genome as: single stranded DNA, single stranded RNA, double stranded DNA, double stranded RNA. Those molecules can be linear, circular, or even consist of multiple individual pieces for a single virus. Most genera of viruses don't even share a single gene in common.

This is nothing like all rodents being similar. At all.

[shunyadragon]

Unreal. You do realize that viruses can store their genome as: single stranded DNA, single stranded RNA, double stranded DNA, double stranded RNA. Those molecules can be linear, circular, or even consist of multiple individual pieces for a single virus. Most genera of viruses don't even share a single gene in common.

This is nothing like all rodents being similar. At all.

ou missed my sarcasm Viruses are both similar and different and regional different.


Waiting for a response.

[shunyadragon]

The point is for you to realize that saying "All viruses are similar" is simply wrong.

. . . because all viruses are viruses. You are making closer comparisons than I when comparing regional viruses like MERS with SARS and COVAG 19. I consider your comparisons simply wrong.

I was looking at the news this morning, and indications that the concept of 'herd immunity' is being considered as possibly explaining the lower intensity of the virus infection in China, the Orient and by the way California. The indication is milder versions of the coronavirus spread out in China and the Orient, and possibly California where large numbers of Chinese travel to the USA. The more virulent COVAG 19 followed. This is different from the 'herd immunity' that develops as result of the infection of the severe infection and vaccines, but in the long term may be related.

I still consider the concept of regional coevolution a possibility as previously cited concerning Herpes viruses, and intimately related to the development of herd immunity proposed now by others.

I want to emphasis that my view has nothing to do with th dangerously 'bogus' concept of 'herd immunity' strategy of just 'letting people get sick and die.' Herd immunity does not stop virus pandemics.

More to follow . . .