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Economic Losses Associated with COVID-19 Deaths in the United States

In addition to the overwhelming health effects of COVID-19, the disease has inflicted unprecedented economic damage. Vast resources have been directed at COVID-19 testing and health care while economic activity has been substantially curtailed due to disruptions resulting from individual choices and government policies. This study estimates the economic loss associated with COVID-19 deaths in the U.S. from February 1, 2020 through July 11, 2020. We use estimates of years of life lost that are based on the age and gender of decedents. Using a value of life year estimate of $66,759, we calculate economic losses of roughly $66 billion. The losses are concentrated in New York and New Jersey, which account for 17.5% of the total losses. Our analysis of per capita losses by state indicates that the highest values are located in the northeastern region of the country, while the values in the western states are relatively low. While economic losses associate with COVID-19 deaths is just one aspect of the pandemic, our estimates can provide context to the value of prevention and mitigation efforts.

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The relevance of antibody waning for the potential for reinfection by SARS CoV-2 is currently not resolved.19,20 During any antibody response to an acute pathogen, some level of antibody waning in the months following infection is expected as short lived plasma cells die. Low levels of affinity-matured antibody usually continues to be produced by long-lived. plasma cells, and may be sufficient to maintain levels of antibody that confer immunity. Indeed for some pathogens such as measles, influenza and rhinovirus, antibodies can be detected for many years after infection. However the situation for coronaviruses is less clear. Human challenge studies showed a more profound waning of serum and nasal antibody over one year following coronavirus challenge than was seen for volunteers challenged with rhinovirus. At one year, re-infection with the seasonal coronavirus was observed whereas volunteers who retained antibodies following rhinovirus infection displayed sterilizing immunity.

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Robust neutralizing antibodies to SARS-CoV-2 infection persist for months
Science 28 Oct 2020

Abstract
SARS-CoV-2 has caused a global pandemic with millions infected and numerous fatalities. Questions regarding the robustness, functionality, and longevity of the antibody response to the virus remain unanswered. Here we report that the vast majority of infected individuals with mild-to-moderate COVID-19 experience robust IgG antibody responses against the viral spike protein, based on a dataset of 30,082 individuals screened at Mount Sinai Health System in New York City. We also show that titers are relatively stable for at least a period approximating 5 months and that anti-spike binding titers significantly correlate with neutralization of authentic SARS-CoV-2. Our data suggests that more than 90% of seroconverters make detectible neutralizing antibody responses. These titers remain relatively stable for several months after infection.

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Antibodies to SARS-CoV-2 can target many of its encoded proteins, including structural and non-structural antigens. Thus far, two structural proteins have been utilized as target antigens for serological assays. One is the abundant nucleoprotein (NP), which is found inside the virus or inside infected cells. However, due to the biological function of NP and the fact that it is shielded from antibodies by viral or cellular membranes, it is unlikely that NP antibodies can directly neutralize SARS-CoV-2. The second structural protein often used as target for characterizing the immune response to SARS-CoV-2 is the spike protein. The spike is a large trimeric glycoprotein that contains the receptor binding domain (RBD), which the virus uses to dock to its cellular receptor angiotensin-converting enzyme 2 (ACE2) and for fusion of viral and cellular membranes (4, 5). It is known from other coronaviruses as well as for SARS-CoV-2 that the spike is the main, and potentially only target for neutralizing antibodies (6).

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After clearance of an infection or effective vaccination, phenotypically distinct B cell populations contribute to short- and long-term humoral immunity. Short-lived antibody-secreting cells (ASC) in blood and secondary lymphoid organs release antibodies into the circulation for weeks to months. Durable humoral immunity (lasting months to years) is mediated by bone marrow-resident, long-lived ASC and by memory B cells (MBC), which rapidly proliferate and differentiate into ASC in response to antigen re-challenge.

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Durable SARS-CoV-2 B cell immunity after mild or severe disease
doi: https://doi.org/10.1101/2020.10.28.20220996

Abstract

Multiple studies have shown loss of SARS-CoV-2 specific antibodies over time after infection, raising concern that humoral immunity against the virus is not durable. If immunity wanes quickly, millions of people may be at risk for reinfection after recovery from COVID-19. However, memory B cells (MBC) could provide durable humoral immunity even if serum neutralizing antibody titers decline. We performed multi-dimensional flow cytometric analysis of S protein receptor binding domain (S-RBD)-specific MBC in cohorts of ambulatory COVID-19 patients with mild disease, and hospitalized patients with moderate to severe disease, at a median of 54 (39-104) days after onset of symptoms. We detected S-RBD-specific class-switched MBC in 13 out of 14 participants, including 4 of the 5 participants with lowest plasma levels of anti-S-RBD IgG and neutralizing antibodies. Resting MBC (rMBC) made up the largest proportion of S-RBD-specific class-switched MBC in both cohorts. FCRL5, a marker of functional memory when expressed on rMBC, was dramatically upregulated on S-RBD-specific rMBC. These data indicate that most SARS-CoV-2-infected individuals develop S-RBD-specific, class-switched MBC that phenotypically resemble germinal center-derived B cells induced by effective vaccination against other pathogens, providing evidence for durable B cell-mediated immunity against SARS-CoV-2 after recovery from mild or severe COVID-19 disease.