Origin of viruses wikipedia

Some recent discoveries of giant viruses have even further complicated the question about the origin of viruses. These discoveries also challenge many of the classical definitions of what makes a virus, such as the size requirement, gene behavior, and how they replicate. Giant viruses were first described in Mimiviruses are different from viruses in that they have way more genes than other viruses, including genes with the ability to replicate and repair DNA. The pandoravirus, discovered in , is even larger than the mimivirus and has approximately genes, with 93 percent of their genes not known from any other microbe.

The pithovirus was discovered in from a Siberian dirt sample that had been frozen for 30, years. However, the pithovirus possesses some replication machinery of its own. While it contains fewer genes than the pandoravirus, two-thirds of its proteins are unlike those of other viruses. Tupanvirus was discovered in Brazil.

It holds an almost nearly complete set of genes necessary for protein production. The discoveries of these giant viruses and others not listed here have made some researchers suggest they lie somewhere between bacterium and viruses, and might even deserve their own branch on the Tree of Life. This would create a yet undescribed fourth domain of life aside from Bacteria, Archaea, and Eukaryotes. You only need to worry if you happen to be an amoeba.

Cholera cannot be eradicated as it is a natural inhabitant of aquatic ecosystems. However, it is estimated that the global burden of cholera is higher due to underreporting. Between and , the number of cases was shown to range between 1. Environmental and climate changes may increase the geographical distribution of cholera Chowdhury et al.

The persistence of cholera is related to poor living conditions including shortage of safe drinking water, insufficient sanitation, crowded housing and the lack of efficient sewage systems. Re-emergence of the disease can also occur following natural disasters such as earthquakes that disrupt access to safe water supply.

Cholera outbreaks could be predicted based on real-time monitoring of oceanic regions, climate fluctuations and epidemiological surveillance program Chowdhury et al. The disease could be prevented by implementation of public health measures to ensure adequate sanitation and safe water supply Somboonwit et al. The access to safe drinking water and sanitation are among the primary priorities of the Millenium Development Goals and the sustainable Development Goals Igere and Ekundayo, These vaccines should be used in areas with endemic cholera, cholera outbreaks and humanitarian crisis with high-risk of cholera in combination with other cholera prevention and control measures World Health Organization [WHO], Cholera is first identified based on clinical symptoms of severe acute watery diarrhea.

The disease is then confirmed by the detection of V. The majority of infected individuals can be treated by the administration of prompt oral rehydration solution. Severely dehydrated patients who are at risk of shock require rapid administration of intravenous fluids as well as antibiotics.

First-line drug consists of doxycycline whereas alternative treatments include tetracycline, ciprofloxacin and azithromycin Hsueh and Waters, Influenza viruses belong to the Orthomyxoviridae family. Influenza viruses are enveloped, negative-sense, single-stranded RNA viruses Wright and Webster, Their genome consists of 7 or 8 RNA segments encoding at least 10 structural and non-structural proteins. Structural proteins include a hemagglutinin HA , a neuraminidase NA , two matrix proteins and a nucleoprotein.

Influenza viruses can be distinguished in types A, B, C, and D. Influenza A and B are responsible for outbreaks in tropical regions and seasonal epidemics in temperate regions whereas influenza A viruses are the only ones with a pandemic potential Lofgren et al. Indeed, influenza A virus is endemic in a number of species including humans, birds and pigs Webster et al. Gene reassortments can thus occur between human and animal influenza A viruses and lead to a new virus subtype which can be pathogenic to humans Webster et al.

In a typical seasonal epidemics, influenza virus causes 3 to 5 million cases of severe illness and approximately , deaths worldwide Iuliano et al.

Most typical seasonal influenza infections are asymptomatic or cause only mild or classical influenza illness characterized by 4 or 5 days of fever, cough, chills, headache, muscle pain, weakness and sometimes upper respiratory tract symptoms Zambon, Among the most severe complications is pneumonia which can be associated with secondary bacterial infection.

Annual influenza epidemics are sustained in the human population through mutations occurring especially in the HA and NA viral surface glycoproteins, the major targets for neutralizing antibodies. Seasonal influenza virus results from frequent antigenic drifts every 2—5 years in response to selection pressure to evade human immunity Kim et al.

Its genome contains segmented genes which may undergo reassortments in cells co-infected with two or more influenza viruses. Each influenza A virus has a gene encoding for 1 of 16 possible HAs and another gene encoding for 1 of 9 possible NAs that are involved in viral attachment and release, respectively Dugan et al. Rarely, antigenic shift which results from reassortment between human and animal viruses leads to the emergence of a new virus subtype Webster et al.

This antigenically distinct virus may have the ability to infect humans and achieve sustained human-to-human transmission and may cause a pandemic if the immunity in the human population is partial or lacking Webster et al. The time in which influenza virus began to infect humans or cause a pandemic cannot be determined with accuracy but many historians agree that the first influenza pandemic could have likely occurred in Morens et al. The Russian flu that occurred between and was the first well-described pandemic Taubenberger et al.

The virus spread rapidly as it took only 4 months to circumvent the planet Valleron et al. The pandemic virus reappeared every year for 3 years and caused an estimated 1 million deaths worldwide Table 1. The median R o was estimated at 2. The case fatality rates ranged from 0. Attack rates were highest in individuals aged 1—60 years and lower in infants and seniors Valtat et al. In contrast, mortality rate showed a J-shape curve with highest rates in infants and people over 20 years of age Valtat et al.

Before its identification, the virus spread silently around the world and its region of origin could not be determined. The — pandemic spread in at least 3 distinct waves within a 9 month interval. The first wave occurred during spring-summer and caused high morbidity and low mortality. Both the second and third waves in summer-fall and winter — caused high mortality. The — influenza pandemic resulted in approximately million infections and 50 million deaths worldwide Johnson and Mueller, However, the — pandemic showed a W-shaped mortality curve with high case fatality rates in the very young and the elderly as well as in healthy young adults aged 20—40 years Morens and Taubenberger, This uncommon age distribution suggests that the severity of the — influenza pandemic was not primarily due to a hyper-virulent strain but was more likely related to host factors that prevent individuals to control the infection.

It is suggested that the influenza virus had an enhanced capacity to spread to and damage bronchial and bronchiolar epithelial cells that could allow bacteria to breach the mucociliary barrier leading to fatal bacterial pneumonia Morens and Fauci, The H1 hemagglutinin of the — pandemic virus was identified as a key virulence factor for mammalian and was associated with increased respiratory epithelial pathogenicity and elicitation of a strong pro-inflammatory response Qi et al.

Most deaths occurred from several days to weeks median 7—10 days after the onset of symptoms Shanks and Brundage, In large cities of Western world, health authorities implemented a series of containment strategies to prevent the spread of the disease including the closure of schools, churches and theaters and the suspension of public gatherings.

Physicians encouraged the practice of individual measures such as respiratory hygiene and social distancing. However, these measures were implemented too late and in an uncoordinated manner due to World War I. Travel restrictions and border controls were impossible to put in place. The movement of military troops and the poor living conditions of soldiers in the trench warfare in Europe facilitated the spread of the disease. Over the past century, descendants of the pandemic virus were the cause of almost all seasonal influenza A epidemics worldwide.

All influenza A viruses responsible for the , and pandemics Table 1 also derived from the founding virus by gene reassortments between human, avian and swine influenza viruses Morens et al. Timeline of influenza pandemics caused by the H1N1 virus and its descendants produced by reassortment of circulating strains with avian influenza viruses AIV and swine H1N1 viruses.

The reassortment of genes is shown in parenthesis. The re-emergence of H1N1 virus in is also shown as it co-circulated with the H3N2 virus before being replaced by the H1N1pdm Sustained transmission of the — pandemic virus started on December with recurrent waves occurring over several years Housworth and Langmuir, The morbidity was highest in children and the mortality was highest at the extremes of age.

The case fatality rate was approximately 0. The global mortality of the — influenza pandemic was estimated at 1—2 millions based on excess death due to respiratory diseases Viboud et al. The R o was estimated at 1. The highest attack rates were in school-age children through young adults up to 35 or 40 years of age Serfling et al. Older adults, including those over the age of 60, had significantly lower attack rates.

This unusual distribution was attributed to the absence of protective antibody among children and middle-aged adults. Histopathological studies from autopsies were characterized by a rapid development of bronchial epithelial necrosis, preservation of the basal layer, limited inflammatory response and evidence of prompt repair Walsh et al.

Secondary bacterial pneumonia was a relatively minor cause of fatalities possibly as a result of the widespread use of antibiotics Robertson et al. The proportion of strains resistant to antibiotics was relatively high in fatal cases compared to those isolated from cases who recovered.

Furthermore, mechanical ventilators were available in the intensive care units ICU to support cases presenting hypoxemia. At that time, the pathogenic agent had been identified Smith and Andrewes, and knowledge on the pathogenesis of the disease had advanced. In , the WHO had implemented a global influenza surveillance network that provided information on the emergence and spread of the novel influenza virus.

Containment measures such as closure of schools and nursery, bans on public gatherings varied from country to country but delayed the onset of the disease for a few weeks only.

The global mortality rate of the — pandemic Hong Kong flu was estimated to be 0. The mean age at death was 62—65 years. The first pandemic season was more severe than the second one in North America whereas the opposite was seen in Europe and Asia Viboud et al. The — influenza pandemic was mild in all countries and comparable to severe seasonal epidemics.

The mildness of this pandemic is expected considering pre-existing immunity to the NA antigen in all age groups and to the HA in the elderly. No specific containment measures were implemented during this pandemic. The H1 protein had minimal antigenic drift compared to its counterpart. Due to its pathogenicity in humans, it is suggested that the maintenance of H1 immunity in the population may be important to prevent future pandemics Morens and Taubenberger, The influenza virus emerged in Mexico and almost simultaneous outbreaks began in Mexico and in Southern United States Neumann and Kawaoka, The virus then spread globally over the next 6 weeks.

Severe disease developed in a small proportion of healthy adults, many of whom had no underlying conditions Viboud et al. The WHO reported 18, laboratory-confirmed deaths. However, the mortality burden was estimated to be between , and , based on excess death due to respiratory diseases in several countries Simonsen et al. The case fatality rate based on confirmed cases was 0.

Later studies estimated the symptomatic case fatality rate at 0. Mortality rates in younger populations affecting children, young adults and pregnant women were higher than in a typical influenza season. The average age of people who died with laboratory-confirmed influenza was 37 years Vaillant et al. Non-pharmaceutical interventions that were implemented included hand washing, use of face masks and cough etiquette Cantey et al.

The pandemic was the first one to combine vaccines and antiviral use. Symptomatic individuals and their contacts were isolated and received antiviral treatment as prophylaxis. Overall, the impacts of an influenza pandemic depend on the transmissibility and virulence of the strain and on the susceptibility of the population, which may vary according to age and past exposure to influenza viruses.

The impacts of influenza are not always higher during pandemics than during seasonal epidemic periods. However, a shift in the age distribution of mortality toward younger age groups distinguishes the impacts of a pandemic from those of seasonal epidemics Simonsen et al. The constant adaptation and exchange of genes between influenza viruses in different species, including at the animal-human interface, is still a critical challenge for the emergence of pandemic viruses nowadays.

In this respect, a series of avian influenza A viruses have caused sporadic cases and outbreaks of severe diseases and deaths in humans Li et al. These viruses are divided into two groups, low pathogenic avian influenza LPAI and highly pathogenic avian influenza HPAI viruses, based on their virulence in chicken.

This virus caused severe and fatal spillover infections in humans and rarely resulted in human-to-human transmission Ungchusak et al. This virus was then shown to evolve to highly pathogenic strains in late Kile et al.

Surveillance programs for monitoring animal influenza viruses with zoonotic potential facilitate the rapid detection of human threats. However, obvious clinical manifestations of influenza infections may be lacking in avian species thereby complicating early detection and efficient control of potential outbreaks Li et al.

Furthermore, the conditions required for cross-species transmission from avian species to humans are not yet elucidated and surveillance programs would most likely require longitudinal surveillance in multiple hosts. Non-pharmaceutical measures aim to reduce the number of live-bird markets and to decrease contacts between humans and birds in breeding facilities have been implemented to prevent and control zoonotic influenza virus infections.

Animal facilities must be periodically disinfected and employees exposed to birds must wear protective personal equipment and be isolated in case of suspected contamination. Pharmaceutical measures include the use of vaccines including poultry vaccination and antiviral agents such as the neuraminidase inhibitors oseltamivir, zanamivir and peramivir and polymerase inhibitors baloxavir marboxil and favipiravir Beigel and Hayden, The WHO together with reference laboratories determine viral antigenicity of strains circulating in avian species that could be used in the development of candidate vaccines for pandemic preparedness.

The development of a universal vaccine to prevent any subtype of influenza virus is a priority Yamayoshi and Kawaoka, As the majority of the population has no protective immunity against the H2 subtype that circulated between and , the emergence of a H2N2 reassortant could be a potential risk for a future pandemic Taubenberger and Morens, Coronaviruses belong to the Coronaviridae family and include four genera, i. Coronaviruses are enveloped, positive-sense, single-stranded, RNA viruses that infect a wide range of animals and humans.

The genome encodes non-structural proteins and 4 structural proteins including the membrane, spike, envelope and nucleocapsid proteins. Human coronaviruses HCoVs cause seasonal respiratory diseases, and to a lesser extent, gastroenteritis. The causative agent was identified within a few weeks Drosten et al. The case fatality rate was 9. Less common symptoms include nausea, vomiting and diarrhea.

Many of these patients also developed watery diarrhea with active virus shedding. Protective immunity against this virus as well as effective antiviral drugs and vaccines were lacking.

The low infectivity and long incubation period viral load peaks at 6—11 days after symptom onset of SARS-CoV provided time for implementing a series of containment measures to prevent transmission Weinstein, Case identification and isolation followed by contact tracing and surveillance proved effective in containing the global threat and eradicating the virus in almost 7 months. Advances in molecular diagnostic tools such as next-generation sequencing allowed that the etiological agent was identified within weeks of global spread Zaki et al.

Those with severe disease are often older than 65 years with comorbidities and can develop symptoms at a later time. Infection with MERS-CoV causes acute, highly lethal pneumonia and renal dysfunction with various clinical symptoms including fever, chills, rigors, headache, a non-productive cough, sore throat, arthralgia and myalgia.

Other symptoms include nausea, vomiting, diarrhea and abdominal pain. The ubiquity of infected dromedary camels close to humans Kandeil et al. The clinical management of patients with MERS-CoV consists mainly in providing supportive care for the relief of pain and fever, supporting vital organ functions and treating concomitant or secondary bacterial infections with antibiotics Memish et al.

Critically ill patients required to be managed in an ICU. Furthermore, this organization has issued recommendations for not consuming unpasteurized camel milk and undercooked animal products and to be cautious in cases of close contacts with dromedary camels. Appropriate hospital hygiene practices and implementation of contact and droplet precautions are crucial to limit future nosocomial outbreaks.

The implementation of extensive contact tracing in order to rapidly diagnose suspected MERS-CoV cases and isolation of individuals to break the chain of infections in the community is also essential. The WHO calls for the development of three types of vaccines against MERS-CoV: a human vaccine that is intended for long-term protection of individuals at high-risk of exposure such as health care workers and those having contacts with potentially infected dromedary camels, a human vaccine for use during outbreaks and a dromedary camel vaccine to prevent zoonotic transmission World Health Organization [WHO], b.

These vaccines are based on DNA, viral vectors, viral proteins, virus-like particles, bacterium-like particles and nanoparticles. Some of the largest known viruses infect simple organisms such as amoebas and simple marine algae. This indicates that they may have an ancient origin, possibly as parasitic life-forms that then adapted to the "virus lifestyle. At the end of the day, however, despite all of their common features and unique abilities to copy and spread their genomes, the origins of most viruses may remain forever obscure.

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Like retroviruses, certain classes of retrotransposons, the viral-like retrotransposons, encode a reverse transcriptase and, often, an integrase. With these enzymes, these elements can be transcribed into RNA, reverse-transcribed into DNA, and then integrated into a new location within the genome Figure 3. We can speculate that the acquisition of a few structural proteins could allow the element to exit a cell and enter a new cell, thereby becoming an infectious agent.

Indeed, the genetic structures of retroviruses and viral-like retrotransposons show remarkable similarities. In contrast to the progressive process just described, viruses may have originated via a regressive, or reductive, process. Microbiologists generally agree that certain bacteria that are obligate intracellular parasites, like Chlamydia and Rickettsia species , evolved from free-living ancestors. Indeed, genomic studies indicate that the mitochondria of eukaryotic cells and Rickettsia prowazekii may share a common, free-living ancestor Andersson et al.

It follows, then, that existing viruses may have evolved from more complex, possibly free-living organisms that lost genetic information over time, as they adopted a parasitic approach to replication. These viruses, which include smallpox virus and the recently discovered giant of all viruses, Mimivirus, are much bigger than most viruses La Scola et al. A typical brick-shaped poxvirus, for instance, may be nm wide and nm long.

About twice that size, Mimivirus exhibits a total diameter of roughly nm Xiao et al. Conversely, spherically shaped influenza virus particles may be only 80 nm in diameter, and poliovirus particles have a diameter of only 30 nm, roughly 10, times smaller than a grain of salt.

Again, poxvirus genomes often approach , base pairs, and Mimivirus has a genome of 1. In addition to their large size, the NCLDVs exhibit greater complexity than other viruses have and depend less on their host for replication than do other viruses. Poxvirus particles, for instance, include a large number of viral enzymes and related factors that allow the virus to produce functional messenger RNA within the host cell cytoplasm.

Because of the size and complexity of NCLDVs, some virologists have hypothesized that these viruses may be descendants of more complex ancestors. According to proponents of this hypothesis, autonomous organisms initially developed a symbiotic relationship. Over time, the relationship turned parasitic, as one organism became more and more dependent on the other.

As the once free-living parasite became more dependent on the host, it lost previously essential genes. Eventually it was unable to replicate independently, becoming an obligate intracellular parasite, a virus. Analysis of the giant Mimivirus may support this hypothesis. This virus contains a relatively large repertoire of putative genes associated with translation — genes that may be remnants of a previously complete translation system.

Interestingly, Mimivirus does not differ appreciably from parasitic bacteria, such as Rickettsia prowazekii Raoult et al. Figure 4 The progressive and regressive hypotheses both assume that cells existed before viruses. What if viruses existed first? Recently, several investigators proposed that viruses may have been the first replicating entities.

Koonin and Martin postulated that viruses existed in a precellular world as self-replicating units. Over time these units, they argue, became more organized and more complex. Eventually, enzymes for the synthesis of membranes and cell walls evolved, resulting in the formation of cells.

Viruses, then, may have existed before bacteria, archaea , or eukaryotes Figure 4; Prangishvili et al. We also know that some RNA molecules, ribozymes, exhibit enzymatic properties; they can catalyze chemical reactions.

Perhaps, simple replicating RNA molecules, existing before the first cell formed, developed the ability to infect the first cells. Villarreal and DeFilippis and Bell described models explaining this proposal. Perhaps, both groups postulate, the current nucleus in eukaryotic cells arose from an endosymbiotic-like event in which a complex, enveloped DNA virus became a permanent resident of an emerging eukaryotic cell.

Where viruses came from is not a simple question to answer. One can argue quite convincingly that certain viruses, such as the retroviruses, arose through a progressive process.

Mobile genetic elements gained the ability to travel between cells, becoming infectious agents. One can also argue that large DNA viruses arose through a regressive process whereby once-independent entities lost key genes over time and adopted a parasitic replication strategy.

Finally, the idea that viruses gave rise to life as we know it presents very intriguing possibilities. Perhaps today's viruses arose multiple times, via multiple mechanisms. Perhaps all viruses arose via a mechanism yet to be uncovered. Today's basic research in fields like microbiology, genomics , and structural biology may provide us with answers to this basic question.

Contemplating the origins of life fascinates both scientists and the general public. Understanding the evolutionary history of viruses may shed some light on this interesting topic. To date, no clear explanation for the origin s of viruses exists. Viruses may have arisen from mobile genetic elements that gained the ability to move between cells.

They may be descendants of previously free-living organisms that adapted a parasitic replication strategy. Perhaps viruses existed before, and led to the evolution of, cellular life. Continuing studies may provide us with clearer answers.