Agent infectious dose

In the case of chemical pesticides, these include factors such as molecular weight and vapor pressure that determine the rate of evaporation into air of the pesticide in an applied material such as paint, or the release from aqueons solntion. In the case of biological agents, these include, for example, pathogenicity to hnmans, allergenicity, infectious dose levels and aerosol particle size distribntion. 

Infectious dose might not be the optimal exposure criterion to use because it is highly dependent upon the methods used for agent preparation and the strain of agent used. 

For chemical toxicants, the dose makes the poison, while for infection agents, the dose is largely irrelevant since even a tiny exposure can multiply in the body For both substances, the dose makes the poison Using PPE for infectious agents is much more important since exposure usually leads to fatality... 

The evaluation of the risks associated with cancer virus research is extremely difficult, since we lack much scientific data on such vital characteristics as agent host range, infec-tivity, host susceptibility, and infectious dose (see Section 11.2). Because the potential consequences of accidental inoculation of laboratory workers with oncogenic viruses are so serious, standards have been developed for work with these agents (476, 477). The technique of risk assessment, which classifies both agents and experimental procedures on the basis of their relative hazards, is very useful for assigning particular ents into hazard categories based upon available data. 

The characteristics of the agent comprise the third element in assessment of risk. Oncogenic agents are classified according to risk based upon criteria established from the evaluation of animal data. The assumption is made that the infectious dose for an animal is related to the hypothetical human infectious dose. For purposes of risk assessment the risk criteria for oncogenic viruses are divided into three categories high, moderate, and low. 

The plaque assay is desirable because it is very sensitive and only detects infectious viral particles. However, there are viral agents which cannot be supported by cell lines. In these cases other methods must be used. The polymerase chain reaction (PGR), which amplifies DNA or RNA from viral agents, can be used to detect the presence and quantity of viral agents. The amount of RNA or DNA target in the initial sample can be determined by competitive PGR where the quantity of amplified product is compared to a control PGR product where the initial amount of target is known. Quantification is also possible by an end-point dilution method similar to that used to determine a tissue culture infections dose. PGR methods can be very sensitive however. 

Clinically, GM-CSF or G-CSF have been used to accelerate recovery after chemotherapy and total body or extended field irradiation, situations that cause neutropenia and decreased platelets, and possibly lead to fatal septic infection or diffuse hemorrhage, respectively. G-CSF and GM-CSF reproducibly decrease the period of granulocytopenia, the number of infectious episodes, and the length of hospitalization in such patients (152), although it is not clear that dose escalation of the cytotoxic agent and increased cure rate can be rehably achieved. One aspect of the effects of G-CSF and GM-CSF is that these agents can activate mature cells to function more efficiently. This may, however, also lead to the production of cytokines, such as TNF- a, that have some toxic side effects. In general, both cytokines are reasonably well tolerated. The side effect profile of G-CSF is more favorable than that of GM-CSF. Medullary bone pain is the only common toxicity. 

To determine if the high in vitro potents of the anti-HIV compound 30 translates into antiviral efficiency in vivo, Datema et al. investigated the inhibition of HIV-1 production and of depletion of human T cells in HIV-1-infected SCID-hu Thy/Liv mice [37]. Steady levels of 100 ng of 30 or higher per mL in plasma resulted in significant inhibition of HIV p24 protein formation. Daily injection of 30 caused a dose-dependent decrease in viral p24 production, and this inhibition could be potentiated by coadministration of AZT (or DDI). This study suggested that 30 alone or in combination with the licensed anti-HIV agents AZT and DDI may decrease the virus load in HIV-infected patients and, by extension, that the infectious cell entry step is a valid target for antiviral chemotherapy of HIV disease. 

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