Recent viral outbreaks of Biblical scale



Infectious diseases are an essential part of our world, affecting virtually every single human being. It is hard to estimate how many times a person gets infected during his life, but still, some statistics could be found in the literature. Every single one of us gets infected by rhinovirus or coronavirus, the causes of the common cold three to four times every year, with children and elderly people even more frequently. Endogenous retroviruses comprise as high as 8% of the human genome, suggesting that infections in the past contributed significantly to the evolution of our species. Infectious and parasitic diseases account for one-quarter of the death cases in the world yearly. However, either due to natural mutations, or engineering on purpose, some pathogens may evolve into highly contagious, devastating pests, able to virtually erase most of the human population. The current paper summarizes some of the deadliest viral diseases, reported in the literature.


Reference: Richard Preston. (1998). The Cobra Event. Random House.

Infectious agent: Chimeric Cobra Virus

Origin: Recombinant virus, resulted from the fusion of nuclear polyhedrosis virus, common cold, and smallpox viruses.

Transmission: Airborne.

Host range: Humans.

Pathogenesis: Starts with common cold symptoms. Later mimic the Lesch-Nyhan syndrome (autocannibalism and aggressiveness toward others) by knocking out the gene for HGPRT (Hypoxanthine-guanine phosphoribosyltransferase), while destroying nerve cells.

Lifecycle:  The virus moves to the central nervous system through the optical and olfactory nerves, where it is the main site of replication.

Prognosis and treatment: Extremely aggressive, with high mortality rate.

Critical assessment: First of all, smallpox is contagious and deadly enough, and considering the ceased vaccination program after its complete eradication (last case reported in 1977), the release of any surviving strain will be worse enough. The inclusion of common cold antigens will not make it more contagious, but it will make it more recognizable to the immune system, therefore allowing more effective immune response. Rhinoviruses (cold) contain RNA genome, while smallpox and the polyhedrosis virus are double strain DNA containing viruses, which will further complicate the engineering process. The smallpox symptoms seem to be missing. Assuming all of that, the Cobra virus does not look like the perfect bio-weapon. Only the inclusion of the polyhedral virus seems appropriate, as it will increase the survival rate outside a host. There are, however, reports that successful chimeras were created between RNA viruses (Ebola) and DNA viruses (Smallpox) during the Soviet Union Biological Weapon program.


Reference: Terry Gilliam. (1995). 12 Monkeys. Universal Pictures.

Infectious agent: Virus, also known as M5-10

Origin: Ancient virus, found in the Annapurna remains. Later, it was engineered and mutated on its own to form even more virulent strains.

Transmission: Airborne and contact

Host range: Humans.

Pathogenesis: Fever, followed by respiratory arrest and internal bleeding.

Lifecycle:  Highly mutable.

Prognosis and treatment: It killed 95 to 99 % (depending on the information source) of the human population in a timeframe between 2016 and 2040. A vaccine may be developed, at least for some of the strains.

Critical assessment: A virus can only survive if a suitable host is available. The lifespan of a virus outside its host is generally measured in hours and strongly depends on the environment. Therefore, it could not be reanimated after thousands of years of sleeping in archaeological remains. It is true that recently a 30 000 years old virus was found to be infectious, but is also true that it was preserved in Siberian permafrost – not damaged because it does not contain cellular structure to be damaged, but preserved from proteases and nucleases, abundant around us. And what about open space? Probably not, because of temperature extremes and high energy radiation.


Reference: Steven Soderbergh. (2011). Contagion. Warner Bros. Pictures

Infectious agent: Meningoencephalitis Virus One (MEV-1)

Origin: Fruit bat and pig viruses combined to form MEV-1

Transmission: Fomites.

Host range: Humans and other mammals.

Pathogenesis: Fever and headache, followed by acute meningitis in a few days.

Lifecycle:  Not specified.

Prognosis and treatment: The mortality rate is approximately 25-30 % and a successful vaccine was developed.

Critical assessment: Too little to say, in fact, this is the typical scenario of zoonotic virus evolution and sounds quite plausible.

Riptide virus

Reference: Bryce Zabel and Jackie Zabel. (2007) Pandemic. Hallmark Channel.

Infectious agent: Virus, H3N7 strain of the bird flu virus

Origin: The pandemic started on a remote Australian beach, spreading out of a colony of sea birds.

Transmission: Airborne

Host range: Humans, birds, dogs, and possibly other vertebrates.

Pathogenesis: Fever and blood vomiting. Death from severe necrosis of the lungs.

Lifecycle:  Similar to other influenza viruses. It also attacks the immune system.

Prognosis and treatment: The incubation period is less than 24 hours, with a high probability of a lethal end or alternatively, the virus may develop in a slower way, allowing a more efficient spread of the disease. Patients with tuberculosis are not infected.

Critical assessment: The virus looks like a mix between bird flu, SARS, and HIV. The possibility that antibodies against tuberculosis would attack the virus is highly improbable, so some other mechanism of acquired resistance must be sought.

Flesh-Eating Virus

Reference: Eli Roth. (2002). Cabin Fever. Lions Gate Film. (And sequels)

Infectious agent: Virus

Origin: Somewhere on a remote island.

Transmission: Mainly by infected blood, sexual contact, or water (both salt and fresh).

Host range: Humans, dogs, and pigs are confirmed hosts.

Pathogenesis: The infection starts with nausea, followed by a rash after 8 to 18 hours. In another hour the skin starts to fall and dead flesh underneath is exposed. Approximately 24 hours after initial exposure are needed for the victim to be doomed.

Lifecycle: Not known, but looks like the virus quickly replicates in most cell types, including mucous membranes and muscle fibers, and destroys them.

Prognosis and treatment: The short incubation period and fast death could generally limit the infection, but the real threat is related to the longevity of the virus in a water environment.

Critical assessment: A typical scenario of a viral outbreak. Such symptoms are more common for a bacterial infection, although it will be less plausible to cause generalized tissue necrosis. Viral necrosis is not common, but this does not mean it is not possible. The viral hemorrhagic septicemia virus or any similar fish virus seems like a good candidate for a virus, which underwent mutation and became infectious to humans.


Reference: Wolfgang Petersen. (1995). Outbreak. Warner Bros.

Infectious agent: Hemorrhagic fever virus.

Origin: Zaire

Transmission: Initially only by contact, later started to transmit by air.

Host range: Humans and capuchin monkeys.

Pathogenesis: It causes fever 4 hours after infection, followed by severe internal and external bleeding and death in about 24 hours.

Lifecycle: Not specified, but almost surely similar to the Ebola virus.

Prognosis and treatment: Lead to a nearly 100% mortality rate in a very short time, so it is considered a major threat to humanity. An antiserum was developed, once for the contact strain and further for the airborne strain. It seems that monkeys are carriers but do not suffer from the same symptoms.

Critical assessment: The virus is fully based on the Ebola virus and other hemorrhagic fevers with the exception it was designed to be faster and deadlier.

Captain Trips

Reference: Stephen King. (1978). The Stand. Doubleday.

Infectious agent: Influenza virus

Origin: Militarized Influenza virus

Transmission: By air and by contact.

Host range: Humans, dogs, rodents.

Pathogenesis: Heavy fever, reddened eyes, and skin, sometimes rashes.

Lifecycle:  Not specified, but typical for an influenza virus. It was further stated, that the virus is highly mutagenic, thus shifting its antigens, and very difficult to cure.

Prognosis and treatment: The mortality rate is 99.4% as experimentally proved because it eradicated exactly this percent of the human population. The incubation period and fatal end vary from several minutes to several days, most probably depending on the current strain, resulting from mutations. About 0.6% of the population appeared to be immune.

Critical assessment: Common flu is bad enough, so I do not think it should be made deadlier in order to produce a weapon. In fact, flu kills around half a million people every season and caused some of the worst pandemics in the history of civilization. It is hard to speculate what exactly the military scientists would change in an influenza virus, as it is one of the most changing viruses, with strains differing due to mutations, rearrangements, or the creation of hybrid viruses of human and avian or swine flu. The killing mechanism might be also different – it usually kills the weak, but the 1918 pandemic was caused by a strain, which killed the healthy through overreaction of the immune system. Overall, the flu pandemic seems a plausible scenario, and it should be also noted that the survivors may have survived because they did not get infected by the suitable strain. Thus, if you are a survivor of a flu pandemic, try to avoid contact with other survivors. Their strain might kill you, and your strain might kill them.

White sickness

Reference: Jose Saramago. (1995). Blindness. Caminho.

Infectious agent: Not specified, most possibly virus.

Origin: Unknown

Transmission: Most probably by contact.

Host range: Humans are confirmed hosts.

Pathogenesis: Proceed asymptomatically until sudden blindness.

Lifecycle:  Similar to many others, the virus enters the central nervous system and specifically affects the optical nerve.

Prognosis and treatment: No specific treatment was developed and a significant percentage of the population was affected.

Critical assessment: There is not much to be said here. Virus-caused blindness is not common, but some cases of complicated herpes infections could lead to this. The best-known blindness-associated disease is trachoma, caused by the bacterium Chlamydia trachomatis, but it takes a lot for it to develop. A new, blindness-causing virus is not impossible and not even exceptional.

The Simian Flu

Reference: Rupert Wyatt. (2011). Rise of the Planet of the Apes. 20th Century Fox.

Infectious agent: ALZ-113 retrovirus strain

Origin: Artificially made in a laboratory as a cure for Alzheimer’s disease.

Transmission: Through the air, contaminated blood, and congenital.

Host range: Humans and apes.

Pathogenesis: Starts with severe headache and weakness in 48 hours, followed by nausea, vomiting, and chest pain in 96 hours. The final stage after approximately 7 days starts with massive bleeding from the nose, mouth, rectum, and eyes. The effect on apes is related to increased intelligence.

Lifecycle: Being a retrovirus, it enters the cells, copies its own RNA into DNA (reverse transcription), and stably integrates it into human chromosomes. Then, it starts to replicate and form new viral particles.

Prognosis and treatment: Approximately 1 in 10 humans possess natural immunity to the Simian flu. Evidently, the almost complete eradication of the human population, accompanied by the raise of apes as civilized, intelligent species left no time for a cure to be developed.

Critical assessment: Retroviruses are a method of choice for gene therapy, as they stably incorporate their own genetic information into human chromosomes and spread it among all infected cells. Thus, if a mutation in a certain gene is the cause of Alzheimer’s disease (just one of several theories), a healthy copy could be incorporated into a retroviral genome and introduced into patients. There are two things that went terribly wrong in this scenario. First, apes, used as test animals developed intelligence. This sounds logical as Alzheimer’s disease is a neurodegenerative process and a gene, responsible for the reversion may also increase the brain efficiency in related species. Second, the virus caused hemorrhagic fever in humans and not in apes. There is a certain mixing of different viruses, as the Ebola-type viruses are RNA-based, but not retroviruses. Anyway, this scenario is also plausible as the Reston Ebola virus causes hemorrhagic fever in primates and asymptomatic infection in humans.

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