Investigation into the Causes and Severity of the 1918 Influenza Pandemic

The 1918 Influenza outbreak is regarded as one of the worst pandemics in human history due to its widespread effects across the globe and its high death rate. This death rate was unusual among influenza infections as most strains do not cause the amount of death that is seen in this outbreak, with 20 million dead as a conservative estimate and 100 million by other estimations. This pandemic was not very well contained for a plethora of reasons. Two main reasons are that it came at a time when understanding viral mechanics still escaped medical professionals, and due to the ongoing war quarantine was not a measure imposed by many cities. To understand how this virus was able to so effectively wreak havoc in the human population, it must be shown how this virus was unique not just in spread, but also in its method of killing its host. These two traits must be looked at together as the virus was able to spread so quickly and this virus was able to kill not just those with a weak immune system, but in many cases those individuals who had the best immune system to fight the infection still died from the disease. The virus was able to be so effective at spreading and causing death, due to alterations to its genome which allowed both for an asymptomatic period of the infection where the PA gene was used as a less pathogenic version (PA-X) this allowed the virus to multiply to a point where it could easily overwhelm total body defense with number of viral particles. This asymptomatic period allowed the viral transmission to spread faster than people expected as the virus would be transmitted before an infected individual knew they were sick. This allowed for another unique trait of the virus to take over, the cytokine storm. This storm used the body’s own defenses to weaken it and paralyze the immune system in a way that allowed for a secondary infection to easily infect the host and cause death. This happened during this pandemic as many of those who died fell to a bacterial pneumonia infection and not the virus itself. These characteristics, combined with the virus’ timing allowed for it to be the worst pandemic that mankind had experienced. As the virus both exhibited novel traits, and came at a time when preventative measures were not in place and human migration was occurring due to the war

Investigation into the Causes and Severity of the 1918 Influenza Pandemic

The 1918 Influenza outbreak is regarded as one of the worst pandemics in human history due to its widespread effects across the globe and its high death rate. This death rate was unusual among influenza infections as most strains do not cause the amount of death that is seen in this outbreak, with 20 million dead as a conservative estimate and 100 million by other estimations. This pandemic was not very well contained for a plethora of reasons. Two main reasons are that it came at a time when understanding viral mechanics still escaped medical professionals, and due to the ongoing war quarantine was not a measure imposed by many cities. To understand how this virus was able to so effectively wreak havoc in the human population, it must be shown how this virus was unique not just in spread, but also in its method of killing its host. These two traits must be looked at together as the virus was able to spread so quickly and this virus was able to kill not just those with a weak immune system, but in many cases those individuals who had the best immune system to fight the infection still died from the disease. The virus was able to be so effective at spreading and causing death, due to alterations to its genome which allowed both for an asymptomatic period of the infection where the PA gene was used as a less pathogenic version (PA-X) this allowed the virus to multiply to a point where it could easily overwhelm total body defense with number of viral particles. This asymptomatic period allowed the viral transmission to spread faster than people expected as the virus would be transmitted before an infected individual knew they were sick. This allowed for another unique trait of the virus to take over, the cytokine storm. This storm used the body’s own defenses to weaken it and paralyze the immune system in a way that allowed for a secondary infection to easily infect the host and cause death. This happened during this pandemic as many of those who died fell to a bacterial pneumonia infection and not the virus itself. These characteristics, combined with the virus’ timing allowed for it to be the worst pandemic that mankind had experienced. As the virus both exhibited novel traits, and came at a time when preventative measures were not in place and human migration was occurring due to the war

Severe Acute Respiratory Syndrome Coronavirus 2 Convalescent Plasma Versus Standard Plasma in Coronavirus Disease 2019 Infected Hospitalized Patients in New York: A Double-Blind Randomized Trial

Objectives: Four peer-reviewed publications have reported results from randomized controlled trials of convalescent plasma for coronavirus disease 2019 infection; none were conducted in the United States nor used standard plasma as a comparator. To determine if administration of convalescent plasma to patients with coronavirus disease 2019 increases antibodies to severe acute respiratory syndrome coronavirus 2 and improves outcome. Design: Double-blind randomized controlled trial. Setting: Hospital in New York. Patients: Patients with polymerase chain reaction documented coronavirus disease 2019 infection. Interventions: Patients were randomized (4:1) to receive 2 U of convalescent plasma versus standard plasma. Antibodies to severe acute respiratory syndrome coronavirus 2 were measured in plasma units and in trial recipients. Measurements and main results: Enrollment was terminated after emergency use authorization was granted for convalescent plasma. Seventy-four patients were randomized. At baseline, mean (sd) Acute Physiology and Chronic Health Evaluation II score (23.4 [5.6] and 22.5 [6.6]), percent of patients intubated (19% and 20%), and median (interquartile range) days from symptom onset to randomization of 9 (6-18) and 9 (6-15), were similar in the convalescent plasma versus standard plasma arms, respectively. Convalescent plasma had high neutralizing activity (median [interquartile range] titer 1:526 [1:359-1:786]) and its administration increased antibodies to severe acute respiratory syndrome coronavirus 2 by 14.4%, whereas standard plasma administration led to an 8.6% decrease (p = 0.005). No difference was observed for ventilator-free days through 28 days (primary study endpoint): median (interquartile range) of 28 (2-28) versus 28 (0-28; p = 0.86) for the convalescent plasma and standard plasma groups, respectively. A greater than or equal to 2 point improvement in the World Health Organization scale was achieved by 20% of subjects in both arms (p = 0.99). All-cause mortality through 90 days was numerically lower in the convalescent plasma versus standard plasma groups (27% vs 33%; p = 0.63) but did not achieve statistical significance. A key prespecified subgroup analysis of time to death in patients who were intubated at baseline was statistically significant; however, sample size numbers were small. Conclusions: Administration of convalescent plasma to hospitalized patients with coronavirus disease 2019 infection increased antibodies to severe acute respiratory syndrome coronavirus disease 2 but was not associated with improved outcome