The avidity with which any virus can cause clinical disease may vary. Like man himself, microbes have proven themselves to be adaptable and inventive, proficient in reproducing and evoking quickly and in adjusting to new hosts and conditions. For example, consider the variation in severity of the various influenza[21] outbreaks over the years. This is a virus which often undergoes major genetic shifts in its surface proteins, thus inflicting a ‘new’ virus on the world at intervals of approximately two years, to which there is little or no immunity in the world population. Such mutations were responsible for a number of flu pandemics, but none more virulent than the Spanish flu of 1918, which, in only six months, killed as many as thirty million people — twice the number that died during the four years of the Great War. This extreme example shows the inherent potential among viruses to change their aggressiveness as the result of spontaneous mutation, although mutations may also occur as the result of outside influences such as chemicals, radiation, bacteria, or even other viruses. The majority of such mutations are corrected rapidly by DNA or RNA-repair enzymes, and do not have the chance to alter the virus activity. Even if not repaired, it is unlikely that the mutations would have an effect on the structure or behavior of the virus in an immediately obvious way. Only one in a million mutations might have a damaging effect on the virus such that it becomes unable to infect cells, or is incorporated in the host cell’s DNA. Conversely, a similar number of mutations might easily result in increased avidity of binding to host cells or more efficient replication of viral products and hence more serious infection and illness. Mutation may also result in a change in the tropism of the virus — in a tendency to attack a cell type not previously affected.
There have been a number of theories as to what caused the relatively benign B19 virus to mutate and become the much more deadly fast HPV1. An increasingly popular theory suggests that an attempt to genetically engineer an antivirus capsid with recombinant DNA technology using a baculovirus system was responsible. Other theories suggest that shortage of blood in Russian hospitals during the early twenty-first century helped encourage their traditional practice of using cadaver blood for infusion, and that B19-infected blood taken from the bodies of people who had been affected by radiation from the Shevchenko[22] disaster of 2011 had mutated to the new form of parvovirus. There has even been the ‘panspermia’ theory, which says B19 met with another virus that had recently arrived from outer space, as detritus from a comet or from a space shuttle. These are only a few of the theories in circulation. What seems certain, however, is that the development of blood substitutes played a significant role in the mutation of B19. Military interest in new battlefield resuscitation solutions that would avoid the logistical problems of whole blood resulted in the creation of a number of products that were reliant on purified bovine hemoglobin, or on bacterial recombinant technology that had used the E. coli organism as a method of expressing human hemoglobin.
Whatever the chain of causation, there can be no argument as to the deadly effect of fast HPV1, which is to eradicate the function of the oxygen-binding site of hemoglobin[23]in otherwise normal people, although there still remains much debate as to how the virus works. Fast HPV1 seems to operate in a choice of three different ways, leading many doctors to believe that fast HPV1 is actually three kinds of parvovirus. These are:
1. the virus causes the defective production of proteins critical for the function of the oxygen-binding site; or
2. the virus turns off the production of such a protein. Oxygen then cannot be transferred by the red cells thus affected; since the lifespan of red cells is one hundred and twenty days, the patient suffocates within this time frame; or
3. codes for the production of blocking polypeptide interact with the active site of oxygen binding.
The second method of operation represents the commonest scenario with fast HPV1. The clinical picture starts slowly with individuals symptom-free for some seven days between the minor febrile period and the appearance of a rubelliform rash; this is followed at four weeks by the sudden onset of symmetrical arthritis affecting the small joints of the hands, followed by wrists, ankles, knees, and elbows; by day sixty patients present symptoms of worsening anemia — fatigue, shortness of breath, cyanosis, confusion; and depending on the general fitness of the patient, fast HPV1 will result in coma and then death by approximately day ninety.
The treatment for fast HPV1 was blood transfusion and the therapeutic use of ProTryptol 14, a specific protease carried in a lipid envelope (or liposome) to prevent premature digestion and targeted at red blood cells. The protease, once released inside the red cell, was designed to act against the mutant protein causing upset at the oxygen-binding site. For many years, however, this formulation was difficult and expensive to produce, and by the time the cost of ProTryptol 14 had come down, the price of whole blood had skyrocketed.
Fast HPV1 was worldwide in distribution and occurred in all populations with the exception of some isolated groups in Brazil and Africa. As with B19, children were the first to be infected, with outbreaks often centered on primary schools, spreading from respiratory tract to respiratory tract. During these first outbreaks, which were always fatal, the parents and teachers of cases also became infected, which led to a second mode of transmission: blood donation. It was the resulting high incidence of virus found in donated units of blood that led to a crisis of confidence in blood donation throughout the Western world, and led also to the widespread creation of autologous blood donation programs. The term ‘bad blood’ has been in use for many centuries, as a way of describing ill-feeling between two people, but never before could this be justified from a physiological viewpoint.
Between 2017 and 2023, fast HPV1 was killing as many as fifty thousand people a day worldwide. Accompanied by a series of natural disasters, from the earthquake that destroyed Tokyo, to the plague of locusts that decimated American agriculture, the Great Middle Eastern War of 2017, and a major eruption of Mount Vesuvius in Italy — not to mention the climatic change that brought a disastrous drought and famine to China — the HPV pandemic was quickly seen by many as a punishment from God. Others blamed the jews, and on the usual tenuous evidence: It had been a Jewish doctor, Benjamin Steinart-Levy, who pioneered ProTryptol 14, which enabled the Goldman Pharmaceutical Company to make billions of dollars during the first months of the pandemic. Pogroms began all over the world, but especially in America; in Los Angeles alone, fourteen thousand Jews were murdered. In New York, when no more bodies could be buried in the city’s cemeteries and parks, Cardinal Martin Walsh blessed the Atlantic so that corpses dumped into the sea would have a consecrated home. Throughout the world, families disintegrated, health-care systems broke under the strain, and countries fell into chaos as governments all but collapsed.
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