7.14: Control of Viruses - Biology

7.14: Control of Viruses - Biology

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Most people don't like having a shot at the doctor's office. They protect you from some very dangerous viruses.

Control of Viruses

People have been able to control the spread of viruses even before they knew they existed. In 1717, Mary Montagu, the wife of an English ambassador to the Ottoman Empire, observed local women inoculating their children against smallpox, a contagious viral disease that was often deadly. Inoculation involves introducing a small amount of virus into a person’s body to allow their body to build up immunity to the virus. This early smallpox inoculation involved putting smallpox crusts into the nostril of a healthy person.


Because viruses use the machinery of a host cell to reproduce and stay within them, they are difficult to get rid of without killing the host cell. Vaccines were used to prevent viral infections long before the discovery of viruses. A vaccine is a mixture of antigenic material and other immune stimulants that will produce immunity to a certain pathogen or disease. The term "vaccine" comes from Edward Jenner's use of cowpox (vacca means cow in Latin), to immunize people against smallpox.

The material in the vaccine can either be weakened forms of a living pathogen or virus, dead pathogens (or inactivated viruses), purified material such as viral proteins, or genetically engineered pieces of a pathogen. The material in the vaccine will cause the body to mount an immune response, so the person will develop immunity to the disease. Smallpox was the first disease people tried to prevent by purposely inoculating themselves with other types of infections such as cowpox. Vaccination is an effective way of preventing viral infections. Vaccinations can be given in schools, shown in the Figure below, health clinics, and even at home. Their use has resulted in a dramatic decline in morbidity (illness) and mortality (death) associated with viral infections such as polio, measles, mumps, and rubella. Genetically engineered vaccines are produced through recombinant DNA technology. Most new vaccines are produced with this technology.

A young student receives a vaccine.

A worldwide vaccination campaign by the World Health Organization led to the eradication of smallpox in 1979. Smallpox is a contagious disease unique to humans and is caused by twoVariola viruses. The eradication of smallpox was possible because humans are the only carriers of the virus. To this day, smallpox is the only human infectious disease to have been completely eradicated from nature. Scientists are hoping to eradicate polio next.

Antiviral Drugs

While people have been able to prevent certain viral diseases by vaccinations for many hundreds of years, the development of antiviral drugs to treat viral diseases is a relatively recent development. Antiviral drugs are medications used specifically for treating the symptoms of viral infections. The first antiviral drug was interferon, a substance that is naturally produced by certain immune cells when an infection is detected. Over the past twenty years the development of antiretroviral drugs (also known as antiretroviral therapy, or ART) has increased rapidly. This has been driven by the AIDS epidemic.

Like antibiotics, specific antivirals are used for specific viruses. They are relatively harmless to the host, and therefore can be used to treat infections. Most of the antiviral drugs now available are designed to help deal with HIV and herpes viruses. Antivirals are also available for the influenza viruses and the Hepatitis B and C viruses, which can cause liver cancer.

Antiviral drugs are often imitation DNA building blocks which viruses incorporate into their genomes during replication. The life cycle of the virus is then halted because the newly synthesized DNA is inactive. Similar to antibiotics, antivirals are subject to drug resistance as the pathogens evolve to survive exposure to the treatment. HIV evades the immune system by constantly changing the amino acid sequence of the proteins on the surface of the virion. Researchers are now working to extend the range of antivirals to other families of pathogens.


  • Several viral diseases can be treated with antiviral drugs or prevented with vaccines.


  1. What is a vaccine?
  2. Describe the relationship between vaccination and immunity.
  3. What diseases can be controlled with vaccinations? List five.

How to stop the spread of viruses

Controlling a virus, especially one as contagious as the novel coronavirus, relies on knowing how it spreads.

For example, the Centers for Disease Control and Prevention (CDC) say that coronavirus spreads by:

  • person-to-person contact
  • the dispersion of infected respiratory droplets into the air when a person with COVID-19 sneezes or coughs
  • a person touching a contaminated surface, such as a counter or doorknob, and then touching their mouth or nose

According to the CDC, the disease is probably most contagious when people are the most symptomatic. However, it is also possible for coronavirus to spread before a person shows any symptoms of COVID-19.

The CDC recommends that people wear cloth face masks any time they are in a public setting. This will help slow the spread of the virus from people who do not know that they have contracted it, including those who are asymptomatic. People should wear cloth face masks while continuing to practice physical distancing. Note: It is critical that surgical masks and N95 respirators are reserved for healthcare workers.

Share on Pinterest Frequent handwashing is one action people can take to stop the spread of viruses.

These practices show what people can do to stop the spread of viruses:

  • Frequent hand washing: This practice helps a person keep any viruses from getting into their body through their mouth or nose. It can also help stop the spread of any viruses that the individual may have contracted.
  • Sanitization: If hand washing is not possible, sanitizers containing at least 60% alcohol can also be helpful. The regular cleaning of shared surfaces, such as doorknobs, can also help stop the spread of viruses.
  • Social distancing: This practice can slow the spread of viruses by keeping people from having close contact with one another.
  • Covering coughs and sneezes: People can use tissues and cough into their elbows, which helps keep infected respiratory droplets out of the air and off surfaces where others could pick them up.
  • Staying at home when unwell: People who do not feel well should stay at home and limit their contact with others to prevent the spread of viruses, even if they have not received a test for the virus.

Businesses can implement the following policies and practices to limit the spread of viruses among employees:

  • encouraging people to work from home if possible
  • telling people who are sick to stay at home and making it financially feasible for them to do so
  • canceling or opting out of large meetings
  • promoting hand washing throughout their offices and facilities, encouraging people to wash their hands for at least 20 seconds with hot water and soap
  • cleaning “high-touch” surfaces frequently
  • providing hand sanitizer and tissues

Social distancing is a public health care practice that officials recommend during disease outbreaks.

The goal of social distancing is to keep people far enough away from each other to prevent the spread of infectious agents, such as viruses.

Social distancing can help stop the spread of viruses, reduce the danger to people most at risk of severe symptoms, and potentially lessen the strain on the health system.

The following are examples of social distancing:

  • encouraging people to keep 6 feet away from others
  • limiting the size of gatherings to no more than a fixed number of people
  • canceling or postponing public festivals, parades, sporting events, and performances
  • canceling face-to-face classes at colleges and universities
  • closing schools
  • avoiding shaking hands and hugging
  • staying at home as much as possible

Although research is limited and mainly model-based, some studies have found that social distancing does lead to a reduction in the rate of infection. However, delayed implementation and poor compliance can reduce its effectiveness.

Even if social distancing is effective in stopping the spread of disease, people can still experience negative emotional and psychological effects, such as increased stress, anxiety, depression, and loneliness.

People can help counteract the potential side effects of social distancing by:


The potential contamination of biopharmaceuticals with adventitious (unintentionally introduced) viruses poses a serious safety risk and threatens public confidence in the use of biopharmaceuticals. This is particularly true in the case of vaccines administered to large numbers of healthy people, including children 1,2 . There have been a number of instances over previous decades where evidence for the presence of adventitious virus contamination in a marketed vaccine product has threatened public trust in immunization programs 3 . Examples include the detection of simian virus 40 (SV40) in the early polio vaccine in the 1960s, the finding of reverse transcriptase in measles and mumps vaccines in 1995 and of porcine circovirus (PCV) nucleic acid sequences and/or infectious circovirus in rotavirus vaccines in 2010 3,4 .

These viruses could be unintentionally introduced at various manufacturing stages and may originate from multiple sources including raw materials, the cell substrate or the environment. Implementation of Good Manufacturing Practise and close monitoring of the manufacturing process can help reduce the likelihood of viral contamination. Therefore, adventitious virus testing at various stages of the manufacturing process is an integral part of the safety assessment for vaccines and other biological products, and there are well-defined regulatory requirements to ensure that these products are absent of adventitious viruses 5,6 .

Gaps exist in the current compendial adventitious virus testing package where some viral families are not detected or incompletely detected by the compendial methods 7,8,9 . Non-specific adventitious virus testing of biological materials has typically included in vivo tests and cell culture-based in vitro tests, the breadth and sensitivity of which are presumed from historical experience rather than from systematic assay validation 9 . In addition, routine testing for adventitious viruses following the compendial requirements generally requires testing the cell substrate and the viral crude harvest (at seed lot and/or bulk levels). Both of these manufacturing stages present complex matrices for in vivo and in vitro testing. Targeted PCR-based virus detection methods require prior knowledge of the adventitious virus with respect to primer design/selection to target specific nucleic acid sequences. As such, there is a need for a broad-range detection method for both anticipated viruses, as well as unanticipated viruses.

A study by the National Institutes of Health (NIH) in 2014 compared the sensitivity of in vivo assays and in vitro cell culture tests using a panel of 16 viruses and found the in vitro tests to be more sensitive for detecting most of the tested viruses 9 . The results from the NIH study support the use of tests for broader detection of adventitious viruses, particularly where no suitable animal models or appropriate culture methods for detection exist. The World Health Organization (WHO WHO technical report series 978 [Annex 3]) 10 and the European Pharmacopoeia (legally binding standards and quality specifications Ph. Eur. 2.6.16, Ph. Eur. 5.2.14, Ph. Eur. 5.2.3.) 10,11,12,13 recommend or require that prior to the implementation of new alternative methods to detect adventitious agents, the specificity and sensitivity of the new and existing methods must be compared and whether the new method has at least the same sensitivity as in vivo methods should be determined (Supplementary Table 1).

High-throughput sequencing (HTS) is a non-specific technique with the potential to detect both known and unknown adventitious agents including viruses 7,14,15,16,17 . High-throughput molecular biology methods (HTS combined with a pan-viral microarray) had succeeded in detecting the contamination of Rotarix vaccine by a porcine circovirus 18 . HTS may also be more sensitive than quantitative PCR (qPCR) 19,20 however the method may be overly sensitive to the detection of background and cross-contaminating viral nucleic acids originating from the laboratory environment or from other sources 21 . Viral genome size can also influence the sensitivity of HTS 22,23 as sensitivity is expected to be proportional to the mass ratio of nucleic acids in a given matrix. Although HTS results for adventitious virus testing may differ between laboratories 24 , the development of well-characterized model virus stocks would support standardization and validation of the different HTS platforms 22 . Currently there are no established viral reference standards with corresponding in vivo data, for assessing new techniques for the detection of adventitious viruses.

The panel of 16 virus stocks from the NIH is instrumental in our efforts to develop, qualify and validate the HTS adventitious virus test, by providing an important baseline against which new techniques for the detection of adventitious viruses can be compared 9 . Here, we describe the development of a general-purpose HTS-based test for the detection of adventitious viruses and its performance using virus stocks equivalent to the 16 NIH model viruses, plus another six viruses of interest. Detection of these viruses was assessed in a live Yellow Fever virus vaccine crude harvest matrix and a Vero cell substrate matrix to define the sensitivity (limit of detection [LOD]) and to demonstrate the specificity of the HTS test for adventitious virus testing.

Book Description

Viruses: Biology, Application, and Control is a concise textbook for advanced undergraduate and graduate students covering the essential aspects of virology included in biomedical science courses. It is an updated and expanded version of David Harper’s Molecular Virology , Second Edition. Focusing on key mechanisms and developments, Viruses presents many new recent scientific advances, including virus evolution, emerging infections, virus extinction, control of infections, antiviral drugs, gene therapy, bacteriophage therapy, and diagnostics.

The first chapters introduce the reader to the structure and nature of viruses, including their classification and evolution. As viruses cause widespread and serious disease, the ensuing chapters explain how they interact with the immune system and the different ways we try to defeat them: vaccines, antiviral drugs, and immunotherapy. Laboratory methods for viral detection and laboratory diagnosis are also covered. While viruses do cause disease, many do not, and their special biology means they can have beneficial uses, and this aspect of viruses is emphasized. One of the most interesting areas in virology, given extensive coverage here, is how new viruses emerge and establish themselves.

Viruses: Biology, Application, and Control is a rigorous treatment of the molecular side of virology and its conceptual approach makes it an essential text for students and non-specialists.

Viral Structure Types

There are many different classification systems for viruses. Viruses can be classified based on the structure of the capsid, genetic material, biological and physiochemical properties, etc. However, most commonly they are classified structurally or morphologically.


TMV Virus Structure (Source: Wikimedia)

Viruses with the helical structure are composed of capsomeres that are identical to each other, and are typically arranged around a central axis, which gives it a helical form.

  • The central portion of this structure can be a hollow cavity. They are also called rod-shaped or filamentous viruses when they appear thin or thread-like.
  • The length and width of the helical capsid depend on the length of the genetic material enclosed within, and on the number of capsomere units that form the capsid respectively. The length ranges from 300-500nm and width ranges from 15-19nm.
  • A classic example of a helical virus is the Tobacco Mosaic Virus or TMV, which is an RNA virus that infects plants. An example of an animal helical virus is the family of viruses called Orthomyxoviridae that causes influenza. Most helical viruses are single-stranded RNA viruses.


Poliovirus Structure (Source: Wikimedia)

Essentially, an icosahedral shape is formed by the fusion of many equilateral triangles spherically. Classic examples of icosahedral viruses include Poliovirus, adenovirus, and rhinovirus.

  • Geometrically, an icosahedral shape has 12 corners or vertices, 20 sides or equilateral triangles and 30 edges.
  • There can be two types of icosahedral capsids – hexagonal at the vertices or pentagonal at the vertices.


Viruses with prolate morphology have an elongated icosahedral shape. This morphology mostly belongs to bacteriophages which are viral particles that attack bacteria.

Head or Tail

Viruses with Head or Tail morphology are a hybrid between icosahedral and filamentous morphological types and basically consist of an icosahedral capsid attached to a filamentous tail. Some bacteriophages possess head or tail morphology of their capsid.

Complex or Asymmetrical

Poxvirus Structure (Source: Wikimedia)

The complex morphological type consists of viruses whose capsid is neither helical nor icosahedral and may be asymmetric. There may be added structures on the outer wall or extra proteins that contribute to this morphological class. The poxvirus is an example of a complex virus due to its unique capsid and outer layer.

Functions of Structure

Here are the functions of virus structure.

  1. The capsid protects the nucleic acid or genetic content from damage such as UV-light or nucleases.
  2. The envelope of the virus aids in the infection process by initiating the attachment process.
  3. Proteins present on the viral capsid as well as envelope help in the delivery of the viral DNA into the host cell.
  4. The different structures and orientations of the capsid provide the virus with rigidity, symmetry, and shape.
  5. The capsid helps in the packaging of the genetic material of the virus.

The structure of viruses is of paramount importance to its life cycle and maintenance of genetic material. Different morphologies and forms of viruses are present that infect a range of host cells across a range of species from bacteria to humans.

It is very interesting to observe how the structure of a tiny non-living particle can impart crucial functions and benefits towards its sustenance.

Types of Influenza Viruses

This is a picture of an influenza virus. Influenza A viruses are classified by subtypes based on the properties of their hemagglutinin (H) and neuraminidase (N) surface proteins. There are 18 different HA subtypes and 11 different NA subtypes. Subtypes are named by combining the H and N numbers &ndash e.g., A(H1N1), A(H3N2). Click on the image to enlarge the picture.

This is a picture of an influenza virus. Influenza A viruses are classified by subtypes based on the properties of their hemagglutinin (H) and neuraminidase (N) surface proteins. There are 18 different HA subtypes and 11 different NA subtypes. Subtypes are named by combining the H and N numbers &ndash e.g., A(H1N1), A(H3N2). Click on the image to enlarge the picture.

There are four types of influenza viruses: A, B, C and D. Human influenza A and B viruses cause seasonal epidemics of disease (known as the flu season) almost every winter in the United States. Influenza A viruses are the only influenza viruses known to cause flu pandemics, i.e., global epidemics of flu disease. A pandemic can occur when a new and very different influenza A virus emerges that both infects people and has the ability to spread efficiently between people. Influenza type C infections generally cause mild illness and are not thought to cause human flu epidemics. Influenza D viruses primarily affect cattle and are not known to infect or cause illness in people.

Influenza A viruses are divided into subtypes based on two proteins on the surface of the virus: hemagglutinin (H) and neuraminidase (N). There are 18 different hemagglutinin subtypes and 11 different neuraminidase subtypes (H1 through H18 and N1 through N11, respectively). While there are potentially 198 different influenza A subtype combinations, only 131 subtypes have been detected in nature. Current subtypes of influenza A viruses that routinely circulate in people include: A(H1N1) and A(H3N2). Influenza A subtypes can be further broken down into different genetic &ldquoclades&rdquo and &ldquosub-clades.&rdquo See the &ldquoInfluenza Viruses&rdquo graphic below for a visual depiction of these classifications.

This graphic shows the two types of influenza viruses (A,B) that cause most human illness and that are responsible for the flu season each year. Influenza A viruses are further classified into subtypes, while influenza B viruses are further classified into two lineages: B/Yamagata and B/Victoria. Both influenza A and B viruses can be further classified into specific clades and sub-clades (which are sometimes called groups and sub-groups).

Figure 1 &ndash This is a picture of a phylogenetic tree. In a phylogenetic tree, related viruses are grouped together on branches. Influenza viruses whose HA genes&rsquo share the same genetic changes and who also share a common ancestor (node) are grouped into specific &ldquoclades&rdquo and &ldquosub clades.&rdquo These clades and sub-clades are alternatively sometimes called &ldquogroups&rdquo and &ldquosub-groups.&rdquo

Clades and sub-clades can be alternatively called &ldquogroups&rdquo and &ldquosub-groups,&rdquo respectively. An influenza clade or group is a further subdivision of influenza viruses (beyond subtypes or lineages) based on the similarity of their HA gene sequences. (See the Genome Sequencing and Genetic Characterization page for more information). Clades and subclades are shown on phylogenetic trees as groups of viruses that usually have similar genetic changes (i.e., nucleotide or amino acid changes) and have a single common ancestor represented as a node in the tree (see Figure 1). Dividing viruses into clades and subclades allows flu experts to track the proportion of viruses from different clades in circulation.

Note that clades and sub-clades that are genetically different from others are not necessarily antigenically different (i.e., viruses from a specific clade or sub-clade may not have changes that impact host immunity in comparison to other clades or sub-clades).

Currently circulating influenza A(H1N1) viruses are related to the pandemic 2009 H1N1 virus that emerged in the spring of 2009 and caused a flu pandemic (CDC 2009 H1N1 Flu website). This virus, scientifically called the &ldquoA(H1N1)pdm09 virus,&rdquo and more generally called &ldquo2009 H1N1,&rdquo has continued to circulate seasonally since then. These H1N1 viruses have undergone relatively small genetic changes and changes to their antigenic properties (i.e., the properties of the virus that affect immunity) over time.

Of all the influenza viruses that routinely circulate and cause illness in people, influenza A(H3N2) viruses tend to change more rapidly, both genetically and antigenically. Influenza A(H3N2) viruses have formed many separate, genetically different clades in recent years that continue to co-circulate.

Influenza B viruses are not divided into subtypes, but instead are further classified into two lineages: B/Yamagata and B/Victoria. Similar to influenza A viruses, influenza B viruses can then be further classified into specific clades and sub-clades. Influenza B viruses generally change more slowly in terms of their genetic and antigenic properties than influenza A viruses, especially influenza A(H3N2) viruses. Influenza surveillance data from recent years shows co-circulation of influenza B viruses from both lineages in the United States and around the world. However, the proportion of influenza B viruses from each lineage that circulate can vary by geographic location.

Figure 3 &ndash This image shows how influenza viruses are named. The name starts with the virus type, followed by the place the virus was isolated, followed by the virus strain number, the year isolated, and finally, the virus subtype.

Naming Influenza Viruses

CDC follows an internationally accepted naming convention for influenza viruses. This convention was accepted by WHO in 1979 and published in February 1980 in the Bulletin of the World Health Organization, 58(4):585-591 (1980) (see A revision of the system of nomenclature for influenza viruses: a WHO Memorandum pdf icon [854 KB, 7 pages] external icon ). The approach uses the following components:

  • The antigenic type (e.g., A, B, C, D)
  • The host of origin (e.g., swine, equine, chicken, etc.). For human-origin viruses, no host of origin designation is given. Note the following examples:
    • (Duck example): avian influenza A(H1N1), A/duck/Alberta/35/76
    • (Human example): seasonal influenza A(H3N2), A/Perth/16/2019

    Influenza Vaccine Viruses

    One influenza A(H1N1), one influenza A(H3N2), and one or two influenza B viruses (depending on the vaccine) are included in each season&rsquos influenza vaccines. Getting a flu vaccine can protect against flu viruses that are like the viruses used to make vaccine. Information about this season&rsquos vaccine can be found at Preventing Seasonal Flu with Vaccination. Seasonal flu vaccines do not protect against influenza C or D viruses. In addition, flu vaccines will NOT protect against infection and illness caused by other viruses that also can cause influenza-like symptoms. There are many other viruses besides influenza that can result in influenza-like illness (ILI) that spread during flu season.

    7.14: Control of Viruses - Biology

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    The coronavirus isn’t alive. That’s why it’s so hard to kill.

    Please Note

    The Washington Post is providing this important information about the coronavirus for free. For more free coverage of the coronavirus pandemic, sign up for our Coronavirus Updates newsletter where all stories are free to read.

    Viruses have spent billions of years perfecting the art of surviving without living — a frighteningly effective strategy that makes them a potent threat in today’s world.

    That’s especially true of the deadly new coronavirus that has brought global society to a screeching halt. It’s little more than a packet of genetic material surrounded by a spiky protein shell one-thousandth the width of an eyelash, and it leads such a zombielike existence that it’s barely considered a living organism.

    But as soon as it gets into a human airway, the virus hijacks our cells to create millions more versions of itself.

    There is a certain evil genius to how this coronavirus pathogen works: It finds easy purchase in humans without them knowing. Before its first host even develops symptoms, it is already spreading its replicas everywhere, moving onto its next victim. It is powerfully deadly in some but mild enough in others to escape containment. And for now, we have no way of stopping it.

    As researchers race to develop drugs and vaccines for the disease that has already sickened 350,000 and killed more than 15,000 people, and counting, this is a scientific portrait of what they are up against.

    ‘Between chemistry and biology’

    Respiratory viruses tend to infect and replicate in two places: In the nose and throat, where they are highly contagious, or lower in the lungs, where they spread less easily but are much more deadly.

    This new coronavirus, SARS-CoV-2, adeptly cuts the difference. It dwells in the upper respiratory tract, where it is easily sneezed or coughed onto its next victim. But in some patients, it can lodge itself deep within the lungs, where the disease can kill. That combination gives it the contagiousness of some colds, along with some of the lethality of its close molecular cousin SARS, which caused a 2002-2003 outbreak in Asia.

    Another insidious characteristic of this virus: By giving up that bit of lethality, its symptoms emerge less readily than those of SARS, which means people often pass it to others before they even know they have it.

    Do viruses evolve to become endemic?

    Despite knowing a lot about the biology of endemic viruses around today, it’s very difficult to work out where they actually came from. Did they always cause these persistent milder illnesses or did they evolve from more severe precursors?

    Viruses replicate really quickly – after entering a host cell, many produce new virus particles within hours. Due to the speed of this process, mistakes are often made in the copying of their genetic material, resulting in mutations.

    Many of these mutations will result in non-viable viruses, unable to infect or replicate. But a small number of these mutations might result in an advantageous change. For example, they may allow the virus to get into host cells quicker or make the jump to a new, different host.

    It’s important to remember these mutations are chance events. Viruses cannot actively decide to mutate or make conscious decisions as to where mutations occur.

    Every time a virus reproduces, there’s a chance it could mutate. ktsdesign/Shutterstock

    Once an advantageous mutation arises, viruses with it can quickly out-compete other versions of the virus to become the dominant form in the population. This is what we think we’re currently seeing with the UK variant, which computer modelling suggests has an increased ability to bind to host cells.

    We can track mutations in current outbreaks, as scientists across the world are regularly recording and analysing the genetic material of virus populations using a process called genomic sequencing.

    However, looking back to determine how today’s endemic viruses changed to take their current genetic form is almost impossible, as it requires looking at the genomes of viruses that no are no longer in circulation. Some historic viruses have been sequenced in the past, but it is rare to find samples well preserved enough to do this – and besides, this gives us more of a snapshot of the virus at a specific time rather than a detailed look back.

    Alternatively, we can look at the genetic material of known viruses now and compare them to each other to try to work backwards to see where certain mutations and strains arose. For instance, the similarity between the endemic coronavirus HCoV-043 and its bovine counterpart, BCoV, implies that the human virus made the jump from cattle. Coupled with historical records, this has led some scientists to propose that the now-endemic HCoV-043 was the cause of a pandemic in the late 1800s.

    There is no direct evidence that pathogens mutate to lose virulence over time, and there is no set roadmap of mutations that allow a virus to become endemic. However, we do know that SARS-CoV-2 is mutating. It’s plausible, but not certain, that it could acquire mutations that help it survive in human populations long term.

    Across a variety of roles and specializations, nursing professionals fight viruses in numerous ways. Some of their methods are direct, such as preventing surgical infections. Others are legislative in nature, such as advocating for care equality by questioning imbalanced care delivery systems. Nurses also share their expertise with the public on a host of vital topics, such as care delivery models, infection prevention and the distribution of important resources.

    Public health nurses were involved in managing the severe acute respiratory syndrome (SARS) outbreak in 2003. They did so by tracing contacts, educating the public regarding disease signs and symptoms and serving in research teams in related case control studies. Nursing researchers have also benefited HIV testing and prevention in Malawi via identifying the benefits of working with religious leaders to promote HIV testing and prevention behaviors. Additionally, nurses have developed family planning services in Kenya by providing childbearing families with the opportunity to space pregnancies to support the health of pregnant women. Finally, nurses have played a key role in West Africa’s Ebola outbreak by improving the protocols and levels of protection for health care workers.

    Slowing the Spread

    Advanced practice nurses are uniquely qualified to conduct research and assist government leaders and public health officials in creating an informed response to viral outbreaks. The input and insight of experienced nurses will help prevent the spread of infectious diseases and ensure a healthier future.

    Watch the video: Τα παράξενα του βρασμού. (August 2022).