COVID-19 has been visiting Mankind since 1962?

1962-2018-Present Day! Some very strange Reports are now showing up about unknown and unidentified Viruses with Spikes for Coronavirus Like Viruses. Could these be our 1st glimpse of the Covid that is here now?

First is from an Article Published in the

Oxford Academic from “2004”. Mere coincidence on all of these Articles or were they all pointing to what was Coming in 2019 and 2020?

https://academic.oup.com/jid/article/189/4/652/839121

However, it has yet to be determined whether this is a favorable format, since the clinical presentation of SARS differs from the assumed clinical presentation of HCoV infection. However, for example, advanced age and underlying disease have also been associated with a more severe presentation of HCoV infection [89]. Also, in case reports, HCoV has been associated with pneumonia after autologous bone marrow transplantation, and we recently identified HCoV by use of nested PCR in the BAL specimen of a severely immunocompromised patient with pneumonia [35]. Interestingly, in the present study, we detected HCoV by realtime RT-PCR in the BAL specimens from 2 patients presenting with severe pneumonia and in the NTSs from patients admitted to the hospital with pneumonia, which again suggests that HCoV may be the cause of severe disease in some patients.

There’s a very Disturbing Article that was Posted in 2018 near the end. It might be of significant importance of COVID-19. A precursor? Maybe all of them were…but some of them were man created for sure…but do tell us more…

Coronavirus (CoV) infection of humans is usually not associated
with severe disease. However, discovery of the severe acute
respiratory syndrome (SARS) CoV revealed that highly pathogenic
human CoVs (HCoVs) can evolve. The identification and character-
ization of new HCoVs is, therefore, an important task. Recently, a
HCoV termed NL63 was discovered in patients with respiratory
tract illness. Here, cell tropism and receptor usage of HCoV-NL63
were analyzed. The NL63 spike (S) protein mediated infection of
different target cells compared with the closely related 229E-S
protein but facilitated entry into cells known to be permissive to
SARS-CoV-S-driven infection. An analysis of receptor engagement
revealed that NL63-S binds angiotensin-converting enzyme (ACE)
2, the receptor for SARS-CoV, and HCoV-NL63 uses ACE2 as a
receptor for infection of target cells. Potent neutralizing activity
directed against NL63- but not 229E-S protein was detected in
virtually all sera from patients 8 years of age or older, suggesting
that HCoV-NL63 infection of humans is common and usually
acquired during childhood. Here, we show that SARS-CoV shares
its receptor ACE2 with HCoV-NL63. Because the two viruses differ
dramatically in their ability to induce disease, analysis of HCoV-
NL63 might unravel pathogenicity factors in SARS-CoV. The fre-
quent HCoV-NL63 infection of humans suggests that highly patho-
genic variants have ample opportunity to evolve, underlining the
need for vaccines against HCoVs.
Coronaviruses (CoVs) are enveloped RNA viruses that are
grouped according to genome sequence and serology (1).
Human CoVs (HCoVs) 229E and OC43 are members of groups
I and II, respectively, and infection with these viruses is thought
to be responsible for 30% of common-cold cases (1). In
contrast, infection with severe acute respiratory syndrome
(SARS)-CoV causes a severe respiratory tract illness (RTI) that
is fatal in 10% of infected individuals (2, 3). The factors that
determine the pathogenicity of CoVs are incompletely under-
stood; however, a role for the spike (S) protein has been
suggested (4). The S proteins of CoVs, which provide virions
with a corona-like appearance, mediate infection of target cells
and play a central role in viral replication (4). The interaction of
CoV S proteins with specific cellular receptors determines, to a
large extent, which cells can be infected (5), and the entry process
is an attractive target for antiviral therapy (6).
Recently, a HCoV termed NL63 was discovered in infants and
immunocompromised adults with RTI (7, 8). HCoV-NL63 is a
group I CoV and is most closely related to HCoV-229E (7–9).
HCoV-229E employs CD13 (aminopeptidase N) as a receptor
for infection of target cells (10, 11). Because the NL63- and
229E-S proteins share 56% amino acid identity (7), it is con-
ceivable that HCoV-NL63 also engages CD13 for infectious
cellular entry. However, the HCoV-NL63-S protein contains a
unique, 179-aa sequence at its N terminus that does not share
homology with other known CoV proteins and that might alter
the receptor specificity of NL63-S relative to 229E-S (7).

Description of Disease


Human coronaviruses (HCV) were discovered in the
1960s during the period of active searching for agents
of the common cold. The first evidence that a new
group of viruses was involved

in human respiratory illness

came from Salisbury, England in 1962,

when volunteers who were given respiratory secretions developed colds;

however, no virus or bacteria could
be isolated in the conventional systems then in use
(Kendall et al., 1962). Further evidence was ob-
tained, although not recognized at the time, when
antibodies to mouse hepatitis viruses (MHV) were
found in human sera (Hartley et aI., 1964). Shortly
thereafter, viruses from the Salisbury study that
were distinct from other known respiratory patho-
gens were grown in human fetal tracheal organ cul-
ture, in which viral replication was evidenced by the
reduction of ciliary activity in the epithelial cells
(Tyrrell and Bynoe, 1965, 1966). Further proof of the
involvement of these new viruses in respiratory dis-
ease was obtained epidemiologically and by volun-
teer transmission studies (Bradburne et aI., 1967;
Tyrrell and Bynoe, 1966).
During this time, another new respiratory virus
was recovered in HEK cells from a group of medical
students in Chicago (Hamre and Procknow, 1966),
and additional viral strains, unrelated to those dis-
cussed previously, were isolated in tracheal organ
cultures from adults in Washington, D.C. (McIntosh
et al., 1967b). The latter were quickly adapted to
suckling mouse brain and were shown to be morpho-
logically identical to MHV (McIntosh et al., 1967a).
In 1967, all of these new viruses were recognized as
morphologically identical to each other and to avian
infectious bronchitis viruses, yet distinct from all
other known viruses (Almeida and Tyrrell, 1967;
Becker et al., 1967; Hamre et aI., 1967; McIntosh et
al., 1967a; Tyrrell and Almeida, 1967).

Because all were characterized by a “corona” of

spikes projecting from the membrane,

they were termed Coronauiruses.

Thus was established a new and distinct
group of viruses, with representative strains already
known to infect mice, humans, and chickens (Tyrrell
et aI., 1968).

But then…

In a study of prophylactic control ofHCV (Turner
et al., 1986), 55 volunteers were given recombinant
interferon intranasally for 15 days and exposed di-

  1. Coronaviridae: The Coronaviruses 475
    rectly to HCV by intranasal inoculation on the 8th
    day. In the placebo group, 73% of the volunteers
    developed colds, compared with 41% in the inter-
    feron-treated group. The interferon also reduced the
    severity of the cold symptoms and shortened the duration of the colds.

1. Introduction

Coronaviruses (CoVs), a genus of the Coronaviridae family, are positive-stranded RNA viruses. The first human coronavirus (HCoV) appeared in reports in the mid-1960s and was isolated from persons with common cold. Two species were first detected: HCoV-229E and subsequently HCoV-OC43 [12]. Since then, more species were described [35].

The HCoV-229E strain was associated with common cold symptoms [6].

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Case Reports in Infectious Diseases+Journal MenuPDFArticle Sections

Case Report | Open AccessVolume 2018 |Article ID 6796839 | https://doi.org/10.1155/2018/6796839Show citation

A Rare Case of Human Coronavirus 229E Associated with Acute Respiratory Distress Syndrome in a Healthy Adult


Foula Vassilara,1Aikaterini Spyridaki,1 George Pothitos,1 Athanassia Deliveliotou,1 and Antonios Papadopoulos2Show moreAcademic Editor: Sinésio TalhariPublished15 Apr 2018

Abstract

Human coronavirus 229E (HCoV-229E) is one of the first coronavirus strains being described. It is linked to common cold symptoms in healthy adults. Younger children and the elderly are considered vulnerable to developing lower respiratory tract infections (LRTIs). In particular, immunocompromised patients have been reported with severe and life-threatening LRTIs attributed to HCoV-229E. We report for the first time a case of LRTI and acute respiratory distress syndrome developed in a healthy adult with no comorbidities and HCoV-229E strain identified as the only causative agent. A 45-year-old female with a clear medical history presented with fever, cough, and headache. Respiratory tract infection was diagnosed, and empirical antibiotics were started. Within two days, she developed bilateral pleural effusions, diffuse consolidations, and ground glass opacities involving all lung fields. She needed immediate oxygen supply, while ABGs deteriorated and chest imaging and PaO2/FiO2 indicated ARDS. Early administration of systemic corticosteroids led to gradual clinical improvement. Multiplex PCR from nasal secretions was positive only for HCoV-229E and negative for multiple other pathogens. It remains to be elucidated how an immunocompetent adult developed a life-threatening LRTI caused by a “benign considered” coronavirus strain, the HCoV-229E.

Molecular Epidemiology of Human Coronavirus OC43 Reveals Evolution of Different Genotypes over Time and Recent Emergence of a Novel Genotype due to Natural Recombination

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3194943/

. This suggested the presence of four HCoV-OC43 genotypes (A to D), with genotype D most likely arising from recombination. The complete genome sequencing of two genotype C and D strains and bootscan analysis showed recombination events between genotypes B and C in the generation of genotype D. Of the 29 strains, none belonged to the more ancient genotype A, 5 from 2004 belonged to genotype B, 15 from 2004 to 2006 belonged to genotype C, and 1 from 2004 and all 8 from 2008 to 2011 belonged to the recombinant genotype D. Molecular clock analysis using spike and nucleocapsid genes dated the most recent common ancestor of all genotypes to the 1950s, genotype B and C to the 1980s, genotype B to the 1990s, and genotype C to the late 1990s to early 2000s, while the recombinant genotype D strains were detected as early as 2004. This represents the first study to describe natural recombination in HCoV-OC43 and the evolution of different genotypes over time, leading to the emergence of novel genotype D, which is associated with pneumonia in our elderly population.

HINDAWI

Published: 15 Apr 2018

1. Introduction

Coronaviruses (CoVs), a genus of the Coronaviridae family, are positive-stranded RNA viruses. The first human coronavirus (HCoV) appeared in reports in the mid-1960s and was isolated from persons with common cold. Two species were first detected: HCoV-229E and subsequently HCoV-OC43 [12]. Since then, more species were described [35].

The HCoV-229E strain was associated with common cold symptoms [6]. Younger children and the elderly were considered more vulnerable to lower respiratory tract infections. Severe lower respiratory tract infection so far has only been described in immunocompromised patients [78]. To our knowledge, there is no report describing life-threatening conditions in immunocompetent adults attributed to HCoV-229E. We report a case of acute respiratory distress syndrome developed in a healthy adult with no comorbidities and HCoV-229E strain identified as the only causative agent.

2. Case Presentation

A 45-year-old female patient presented to the emergency department with dry cough, headache, and fever up to 39.5°C lasting a few hours. Her past medical history was unremarkable, and she did not take any medication regularly. She has never smoked, worked as a teacher at a local high school, and has not recently travelled.

Clinical examination revealed rales at her left lower lung fields. Chest X-ray showed diffuse opacities and consolidation at this field. The arterial blood gases (ABGs) were normal, and intravenous ceftriaxone and azithromycin were empirically administered for lower respiratory tract infection (LRTI). S. pneumoniae and L. pneumophila antigen in the patient’s urine specimen was negative, and blood cultures were sterile.

Over the next two days, the patient’s clinical condition rapidly deteriorated, with development of tachypnea (34 respirations/minute), dyspnea, and hypoxemia. ABGs changed to PaO2 of 55.3 mmHg, PCO2 of 31.4 mmHg, and pH of 7.487. Lung auscultation revealed diffuse rhonchi symmetrically all over her chest, bronchial breathing at her right and left lower lobes, and diminished vesicular sounds. Chest CT scan displayed bibasilar pleural effusions and diffuse consolidations plus ground glass opacities involving all lung fields (Figure 1). Oxygen was supplied at 5 L/min, and antimicrobial therapy was changed to levofloxacin 500 mg/day. Systemic corticosteroids and bronchodilators were added about 40 hours after her hospitalization. Samples of the pleural fluid showed exudate with 260 cells/mm3, negative Gram stain, and sterile cultures.(a)
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