NUR 200 Clinical Week 5
Assignment
Learning Objectives
1. Demonstrate effective use of technology to conduct a literature review of Covid-19 to obtain evidence-based articles from reliable peer review nursing journals. (EBP, Informatics)
2. Summarize evidence-based practice presented in the peer review nursing journal. (EBP)
3. Apply evidence-based practice to nursing practice today. (EBP, Safety, Patient Centered Care, Practice)
4. Correlate a QSEN competency with current trends in healthcare related to COVID 19/nursing practice with an appropriate journal article. (Patient-Centered Care, Teamwork & Collaboration, EBP, Quality Improvement, Safety, Informatics)
5. Review a journal article summary of a peer and make related comments and suggestions. (EBP)
Assignment
This assignment is designed to teach students how to develop research and application skills through formal review of literature related to a current trend in health care (Covid-19 Pandemic). Current event must pertain to one of the six competencies of Quality and Safety Education for Nurses (QSEN)
(click here for competencies)
. The area of interest, clinical issue, or research problem must focus on current nursing trends directly related to Covid-19.
The article for summary must be approved by clinical instructor. Once approved, students are to write a professional summary of the chosen article. The summary should describe relevance to your chosen QSEN competency and how the findings impact nursing practice. Summaries must follow APA guidelines and are to include a title page, article summary page, and reference page (example video uses MLA – you must use APA).
Once completed, students are to perform a peer review of summary. Your assigned peer reader is
listed here
. This must be emailed to your peer and clinical instructor no later than 4/28 by noon. Peer is to proof document, add corrections/suggestions as needed, and email updated doc to back to student and clinical instructor by noon on 4/29. Student is to make corrections, as needed, and submit via D2L by 4/30 at 08:00. Your finished summary should be of quality that you could present at a DTCC nursing student related event.
Evaluation
Evaluation of the learning objectives is completed through earning a passing grade on the completed written assignment. Through this project, students are able to identify QSEN competencies while identifying how patient care can be improved utilizing current evidence-based practice protocols.
Resources
Example of Assignment:
Johnny reviews QSEN competency categories and has an interest in safety and emergency nursing. Johnny does a literature review of all safety issues related to Covid-19 and emergency room nurses. Johnny finds a peer-reviewed journal article on emergency nursing and lack of PPE while treating Covid-19 patients. Johnny writes a summary of article in APA and emails it to Joanie, his assigned peer proof reader, and cc’s Andria, his clinical instructor. Joanie writes her suggestions for editing and emails this back to both Johnny and Andria. Johnny makes edits and submits final draft to D2L before submission due date.
An APA summary has four crucial components:
1. 1. An original peer reviewed research article (
click here for example of peer reviewed article
). Make sure you have the full-text of the article (can use DTCC library website or Christiana Care Medical Library website).
2. Your summary (
click here to learn how to do summary
) of the original research article.
3. The APA for original research article (
click here for APA
).
4. Have an outside reader proof your writing – use your assigned student in your clinical group
(listed here)
.
EDITORIAL Open Access
Can an effective SARS-CoV-2 vaccine be
developed for the older population?
Graham Pawelec1,2* and Nan-ping Weng3*
The emergence of SARS-CoV-2 and its inordinately rapid spread is posing severe challenges to the wellbeing of
millions of people worldwide, health care systems and the global economy. While many younger people
experience no or mild symptoms on infection, older adults are highly susceptible to life-threatening respiratory and
systemic conditions which demand a full understanding and leveraging of knowledge of the differences between
immunity in young and old people. Consequently, we welcome papers addressing any issues relevant to immunity
and ageing in the context of SARS-CoV-2, and will endeavour to fast-track peer-review. We aim to provide a
platform exclusively for discussions of individual and age differences in susceptibility and immune responses to
COVID caused by SARS-CoV-2 infection and how to prevent or reduce severity of disease in older adults.
Keywords: Severe acute respiratory syndrome, SARS-CoV-2, Immunosenescence, Vaccination, COVID
The newly-emerged Coronavirus SARS-CoV-2 is highly
infectious and has rapidly spread throughout the world
with a case fatality rate (CFR) highly dependent on age
and pre-existing conditions associated with age. As more
data become available, average CFRs in children appear
negligible, in young adults perhaps up to 1%, but in
people over 60 rising to 4%, over 70 up to 9% and over
80 even up to 18% (see, for example, https://www.cebm.
net/covid-19/global-covid-19-case-fatality-rates/).
Clearly, these figures can vary tremendously from coun-
try to country, and depend on the state of health of the
patients and the state of the health care system, but it is
likely that this sort of age stratification reflects the gen-
eral characteristics of Coronavirus disease (COVID). Ob-
viously, there is vigorous debate as to why this may be,
but a common denominator is the waning of immunity
with age. Although much effort is currently directed at
repurposing licensed drugs as anti-virals, particularly
those with anti-inflammatory effects [1] this is usually
viewed as a stop-gap measure and hopes are pinned on
developing effective vaccines. An unprecedented world-
wide effort is channelling academic and industrial re-
sources into the rapid production and testing of SARS-
CoV-2 vaccines. Quite apart from the potential dangers
of accelerated vaccine development [2], and remember-
ing the additional danger of immune enhancement [3],
even were this successful the question remains whether
the most susceptible members of the population (say,
those over 60) would benefit.
COVID immunopathology and potential interventions
There is no pre-existing immunity to a virus not previ-
ously encountered except via cross-reactivity or shared
viral antigen, as is sometimes the case for seasonal influ-
enza strains. As SARS-CoV-2 is almost certainly com-
pletely novel for at least the vast majority of people, the
virus enjoys unrestrained entry into host cells which
then rely on intracellular (cell-intrinsic) anti-viral de-
fence mechanisms [4]. If these fail, cell death releases
damage-associated molecules (DAMPs) and viral parti-
cles triggering inflammatory reactions. Severe acute
© The Author(s). 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License,
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appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if
changes were made. The images or other third party material in this article are included in the article’s Creative Commons
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permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the
data made available in this article, unless otherwise stated in a credit line to the data.
* Correspondence: graham.pawelec@uni-tuebingen.de;
wengn@grc.nia.nih.gov
1Department of Immunology, University of Tübingen, Tübingen, Germany
3National Institute on Aging, Baltimore, MD, USA
Full list of author information is available at the end of the article
Pawelec and Weng Immunity & Ageing (2020) 17:8
https://doi.org/10.1186/s12979-020-00180-2
http://crossmark.crossref.org/dialog/?doi=10.1186/s12979-020-00180-2&domain=pdf
http://creativecommons.org/licenses/by/4.0/
http://creativecommons.org/publicdomain/zero/1.0/
mailto:graham.pawelec@uni-tuebingen.de
mailto:wengn@grc.nia.nih.gov
respiratory syndrome is caused by dysregulated over-
exuberant inflammatory responses that can progress to a
systemic sepsis-like “cytokine storm” [5], which together
with effects of the virus also directly infecting other or-
gans, not just the lung, can result in multiple organ fail-
ure. The aim of prophylactic vaccination of course is to
induce sufficient neutralising antibody to prevent infec-
tion and sufficient numbers of virus-specific resident
memory cytotoxic T cells in the lung to prevent viral
replication. This requires the presence and efficient co-
operation of antigen-presenting cells, T cells and B cells
within a correctly functioning microenvironment (lymph
node). When vaccination is unable to elicit qualitatively
or quantitatively sufficient protective antibody, host cell
infection will still take place, and may trigger sequelae
described above. Given the rapidity and degree with
which SARS-CoV-2 can cause immunopathology in the
lung, vaccines would have to be highly efficient in gener-
ating neutralising antibody as well as protective cell me-
diated local immunity to prevent this sequence of
events. Achieving such immune protection by a vaccine
is quite feasible in the young, but it may prove to be
challenging in old populations as evidenced by the low
efficacy of seasonal influenza vaccine in such popula-
tions. Alternatively, adoptive immunotherapy with neu-
tralising monoclonal antibody, as in cancer treatment,
may be a possibility, and several companies are working
on this. However, repeated i.v. infusion of sufficient anti-
body does not seem a priori an optimal approach.
Clearly, traditional vaccination to stimulate the patient’s
own response would be preferable, but how likely is it
that that could be accomplished in older people?
Immunosenescence and its underlying mechanisms
Altered immune competence with increasing age, so-
called immunosenescence [6], is the result of changes at
multiple levels of the immune system over time. It in-
cludes the altered balance of immune cell production in
the bone marrow resulting in reduced lymphopoiesis
and increased output of myeloid lineage cells which are
also functionally compromised. Thymic involution sub-
stantially reduces the output of naïve T cells and the
TCR repertoire contracts over time. Although loss of cir-
culating naïve B cells is less profound than naïve T cells,
reduced BCR repertoire diversity with age is also well
recognized. Furthermore, aging is associated with the
dysfunction of innate immune cells like neutrophils at
sites of infection possibly due to the poorer capacity of
the adaptive immune system to reign in over-exuberant
inflammatory responses. The ability to generate adaptive
immune responses is compromised by dysfunction of
antigen-presenting cells and disorganised and fibrotic
lymph node architecture. Collectively, these changes pre-
vent appropriate control of the initial inflammatory
response and decrease the generation of an efficient and
robust adaptive immune response which requires the
production of large number of functional effector T cells
and B cells. For all these reasons, protective responses to
infection or vaccination tend to be on average lower in
many older adults than in the young, but there is enor-
mous inter-individual variation in people owing to the
individual variations of genetics and the history of envir-
onmental exposures. Hence, two crucial questions are
raised by these considerations: 1) how can we measure
immune and physiological status in an individual in a
clinically meaningful manner and 2) how can we inter-
vene at the crucial checkpoints thus identified in order
to restore appropriate immune function? Identification
of biomarkers of protective or detrimental responses to
a SARS-CoV-2 infection or vaccine and determination
of the kinetic pattern of these biomarkers during the
course of infection or vaccine response are critical to ad-
dress these questions.
Biomarkers and vaccine requirement
There are few precedents to assist us here. Efforts to de-
velop a prophylactic vaccine or SARS-CoV-1 were shelved
when the infection faded by itself. There are surprisingly
few data available concerning the status of immune respon-
siveness to truly novel antigens in humans. A study on Yel-
low Fever vaccination of the elderly pointed to
dysfunctional antigen-presenting cells and a dearth of
antigen-specific CD4+ Th helper cells as culprits in the low
antibody responses of older vaccinees [7]. Otherwise, we
have to rely mostly on the large literature on seasonal influ-
enza vaccination. However, the problem here is that every-
one has already been exposed to some strains of influenza
and even newly-emerging strains such as the avian H7N1
are not entirely novel. Nonetheless, knowledge garnered on
immunity and responses to vaccination against this virus
may tell us something about the capacity of older adults to
respond to SARS-CoV-2. Primate models featuring the re-
sponses of older monkeys to SARS-CoV-1 infection may
also be informative [8]. A systems biology approach will be
needed to identify the protective antigen/epitopes of SARS-
CoV-2 for both antibody/B cell responses and T cell re-
sponses and to classify them as protective or non-protective
responses to serve as useful biomarkers. Importantly, vac-
cine design for the older adult should aim to stimulate a
broad T and B cell response potentially overcoming re-
duced immune function in the older population.
How can current immunological knowledge be leveraged
to protect the oldest old against COVID?
According to the above arguments, we consider it un-
likely that a conventional vaccine based on young adult
responses will be highly effective in COVID prophylaxis
for older adults, but should be rigorously applied to
Pawelec and Weng Immunity & Ageing (2020) 17:8 Page 2 of 3
everyone else to achieve herd immunity that will indir-
ectly protect the elderly. The ability to prevent infection
by adoptive immunotherapy remains a possibility, albeit
logistically and financially challenging. Pharmacological
prevention of infection by other means, for example, by
blocking the interactions between viral proteins and host
cell molecules acting as receptors may be useful. Finally,
various ways to improve the general immune functions
in the older population should be considered and devel-
oped to strengthen the immune response to infection
and vaccine in general. These approaches could include
interventions at the level of hematopoiesis to correct the
skewing of output towards dysfunctional myeloid cells
responsible for acute inflammatory responses in the
lung, normalisation of T cell progenitor output and re-
constitution of the thymus for correct selection of T
cells, especially regulatory T cells to keep inflammation
in check, reconstitution of antigen presentation function
in the lymph nodes and re-alignment of T-B cell interac-
tions and functionality. In the meantime, the major
benefit of vaccination will be seen at the population level
in younger people. Once herd immunity is established,
the well-known effect of diluting out new hosts for acute
viruses should result in the virus disappearing, with the
proviso that protective immunity is retained for long
enough (this is not yet established) and reinfection is not
introduced from a location where new hosts were still
available. And with the linked proviso that the virus does
not mutate into a form against which immune memory
is not present.
We welcome papers addressing any of the issues dis-
cussed above and will endeavour to fast-track peer-
review to provide a platform exclusively for discussions
of individual and age differences in immune responses
SARS-CoV-2 and susceptibility to COVID and how to
prevent or reduce severity of disease in older adults.
None.
Both authors wrote and revised the manuscript. The author(s) read and
approved the final manuscript.
No further information.
No specific funding.
Not applicable.
Not applicable.
Both Co-Editors-in-Chief consent to publication.
Both authors declare no competing interests.
1Department of Immunology, University of Tübingen, Tübingen, Germany.
2Health Sciences North Research Institute, Sudbury, Ontario, Canada.
3National Institute on Aging, Baltimore, MD, USA.
Received: 31 March 2020 Accepted: 3 April 2020
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- Abstract
Introduction
COVID immunopathology and potential interventions
Immunosenescence and its underlying mechanisms
Biomarkers and vaccine requirement
How can current immunological knowledge be leveraged to protect the oldest old against COVID?
Acknowledgements
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