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Persistent and Slow Virus Infections

Lymphocytic choriomeningitis (LCM) viruses isolated from the blood of persistently infected mice, could be clearly divided into two categories by observing the disease patterns they produced after intracerebral (i.c.) injection in a number of adult inbred and outbred mice. One type (aggressive) caused the classic pattern of convulsive death in 100% of the mice 7 to 9 days after infection, while the other (docile) caused a protracted disease with deaths occurring, if at all, 2 to 4 weeks after infection. Interferon could be detected in the serum of adult mice on the 3rd and 4th day after infection with several independently cloned aggressive, but not docile, viruses. The inability of docile virus to induce interferon was not due to poor or delayed virus replication in the brain. The aggressive pattern of disease could be provoked easily in docile virus-infected mice with the interferon inducers poly(rI) . poly(rC), tilorone hydrochloride or Newcastle disease virus. The amount of interferon produced had little effect on the mean day of death. Mice that differed over 10-fold in their serum interferon levels after LCM infection, either by genetic predisposition or by stimulation with increasing amounts of poly(rI) . poly(rC), presented almost identical patterns of mortality.

Interferon induction by lymphocytic choriomeningitis viruses correlates with maximum virulence.

Several, structurally different, copper-binding ligands can inhibit the RNA-dependent DNA polymerase of Rous sarcoma virus (RSV) and can inactivate the ability of the virus to malignantly transform chick embryo cells. These ligands include the anti-microbial agents, thiosemicarbazones, 8-hydroxyquinolines, isonicotinic acid hydrazide, and others. Many of these compounds bind to DNA and RNA in the presence of copper, which may play a role in their anti-viral activity. However, not all agents active against RSV bind to nucleic acids and not all ligands that bind to nucleic acids are active against RSV. Some copper-binding ligands are neither active against RSV, nor bind nucleic acids. It appears that there is no simple relationship between the anti-viral activity of copper-binding ligands and their nucleic acid-binding ability. The biological importance of thiosemicarbazone-copper complex binding to nucleic acids is supported by the observation that treatment of intact RSV virions with the complex causes the genome 70S RNA to sediment abnormally in velocity sucrose gradient analysis.

Anti-Tumor Virus Activity of Copper-Binding Drugs

The dihydrochloride salt of ( S,S )-1,2-bis(5-methoxy-2-benzimidazolyl)-1,2-ethandiol (A37536) inhibits the synthesis of lymphocytic choriomeningitis (LCM), Parana, and Pichinde viruses in L-929 cells. The compound has no direct inactivating effect on LCM virus nor does it affect the adsorption of LCM virus to L cells. The drug-cell interaction is slow. Maximal activity is observed only by exposing cells to the drug at least 8 h prior to LCM virus infection, or by concomitant drug treatment and infection at a low multiplicity. Addition of serum-free media to L cells after LCM virus infection diminishes the activity of A37536. Whereas A37536 exhibits its antiviral activity at concentrations that have little or no effect on L cell division rate, a marked change can be noted in the cell9s sensitivity to lysis by standard trypsin dispersal procedures. A37536 has no specific antiviral activity in LCM virus-infected BHK, HeLa, or Vero cells. All of the four tested derivatives of A37536 showed antiviral activity against LCM virus but only at concentrations that reduced the growth rate or were toxic to L cells.

Characteristics of the in vitro inhibition of arenavirus synthesis by bis-benzimidazoles.

Two groups of compounds, identifiable by structural similarity, have been found to interfere with the in vitro replication of arenaviruses. All 4 members of the benzimidazole group contain dipolar fused benzene and 5-membered nitrogen-containing rings and share potential chelating ability through the different bidentate structures formed with their side-chains. The biological activity of one of these compounds, metisazone, has been shown to depend on the presence of divalent metals of the first transition series, Cu++ being the most effective. Furthermore, whereas metisazone inactivates cell-free virus, two other members of the group, HBB and 1,2-bis(5-methoxy-1H-benzimidazol-2-yl)-1,2-ethanediol, act intracellularly. The site of action of the fourth member, SKF 30097, is not known. Using murine lymphocytic choriomeningitis infections as an in vivo model, the bisbenzimidazole derivative has been found to increase life-span without interfering with virus replication. Medication with SKF 30097 or metisazone and copper (2+) sulfate did not significantly or reproducibly change the expected day of death of the animals. The amantadine compounds of the second group have unusual symmetric structures with a 10-carbon cage. The parent compound acts intracellularly, while the site of action of an octachloro derivative is not known. Medication with the parent compound, but not the derivative, shortened the interval between LCM infection and death of the mouse. Tissue culture and animal screening of the many available derivatives in these two groups may uncover compounds more efficacious than those already examined.

Arenavirus chemotherapy—retrospect and prospect

Seventy percent of the mice receiving (S,S)-1,2-bis(5-methoxy-2-benzimidazolyl)-1,2-ethandiol (A36683) in their drinking water lived at least four times longer than control mice when infected with 10 or 100 mean lethal doses of lymphocytic choriomeningitis virus strain UBC. In the next 4 months, most of the survivors died with lymphocytic choriomeningitis-like symptoms. Drug treatment during the first 7 days after infection was found to have no significant effect on virus titers in various organs. The sparing effect of the drug is discussed in terms of immunosuppression.

Evaluation of Bis-Benzimidazoles in the Treatment of Murine Lymphocytic Choriomeningitis Virus Infections

Evaluation ofBis-Benzimidazoles intheTreatment ofMurine Lymphocytic Choriomeningitis Virus Infections

Optimizing vaccination to reduce COVID-19 death remains a challenge. A new method, Gompertzian Analysis, examines numbers of infectious disease cases and deaths, by age, on log graphs, capturing COVID-19 Lethality (Deaths/Cases) by the Gompertz Mortality Equation. Gompertzian Analysis revealed that each of the first 4 Vaccination Events (primary and boosters) led to a [~]1/3rd reduction in COVID-19 Lethality. These vaccination reductions in COVID-19 Lethality were cumulative, persistent, and undiminished by variants, while vaccinations impact on COVID-19 Infectivity (Cases/Population) was fleeting. Primary vaccination and 3 boosters gave an [~]85% reduction in COVID-19 Lethality, with projections suggesting [~]68% fewer deaths ([~]267,000 to [~]85,000). Projections also suggest that 6 boosters may offer a [~]96% reduction in COVID-19 Lethality, to the familiar level of influenza, with a [~]91% reduction in COVID-19 deaths, to [~]25,000, fewer than automobile deaths. Gompertzian Analysis provides rational vaccination guidelines by age. Gompertzian Analysis points to a strategy molded by multiple vaccinations reducing COVID-19 Lethality, which is persistent, rather than focusing on reducing COVID-19 Infectivity, which is fleeting. Such a strategy, based on accumulating the necessary number of vaccinations ([~]7), and possibly no more, would accept vaccinations limited ability to prevent infection in exchange for its power to prevent death.

https://www.medrxiv.org/content/medrxiv/early/2023/04/15/2023.04.14.23288579.full.pdf

A New Vaccination Assessment Method and Strategy for COVID-19

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Author Correction: Protein interaction network of alternatively spliced isoforms from brain links genetic risk factors for autism

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Evaluation of Bis-Benzimidazoles in the Treatment of Murine Lymphocytic Choriomeningitis Virus Infections

Evaluation ofBis-Benzimidazoles intheTreatment ofMurine Lymphocytic Choriomeningitis Virus Infections

A New Vaccination Assessment Method and Strategy for COVID-19

Author Correction: Protein interaction network of alternatively spliced isoforms from brain links genetic risk factors for autism