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Acute toxicity of a chemical can be viewed from two perspectives. Acute toxicity may be the descriptor used as a qualitative indicator of an incident of poisoning. Consider the following statement: methyl isocyanate gas, accidentally released from a chemical manufacturing facility in 1984, was acutely toxic to the residents of Bhopal, India. This statement implies that the residents of Bhopal were exposed to suf ciently high levels of methyl isocyanate over a relatively short time to result in immediate harm. High-level, short-term exposure resulting in immediate toxicity are all characteristics of acute toxicity. Alternatively, acute toxicity may represent a quanti able characteristic of a material. For example, the statement: the acute toxicity of methyl isocyanate, as measured by its LD50 in rats, is 140 mg/kg de nes the acute toxicity of the chemical. Again, the characterization of the quanti ed effects of methyl isocyanate as being acute toxicity implies that this quanti cation occurred during or following short-term dosing and that the effect measured occurred within a short time period following dosing. In terms of these qualitative and quantitative aspects, acute toxicity can be de ned as toxicity elicited immediately following short-term exposure to a chemical. By this de nition, two components comprise acute toxicity: acute exposure and acute effect.

FIGURE 11.1 The hepatitis delta virus (HDV) life cycle and the role of prenylation. (a) The HDV life cycle begins with infection of a human hepatocyte (1). Upon entry, the viral particle is uncoated (2) and the genome with associated core-like delta antigens is transported to the nucleus (3), where replication (4) is mediated by small delta antigen (SHDAg). An RNA editing event that occurs during replication gives rise to the production of large delta antigen (LHDAg). LHDAg undergoes prenylation [detailed in part (b) of the gure]. The latter is necessary for assembly (5) and release (6) of new progeny viral particles in

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In contrast to acute toxicity, chronic toxicity is characterized by prolonged exposure and sublethal effects elicited through mechanisms that are distinct from those that cause acute toxicity. Typically acute and chronic toxicity of a chemical are easily distinguished. For example, mortality occurring within two days of a single dose of a chemical would be a prime example of acute toxicity (Figure 11.1a). Similarly, reduced litter size following continuous (i.e., daily) dosing of the parental organisms would be indicative of chronic toxicity (Figure 11.1b). However, de ning toxicity as being acute or chronic is sometimes challenging. For example, chronic exposure to a persistent, lipophilic chemical may result in sequestration of signi cant levels of the chemical

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There are hundreds of interferon-stimulated genes (ISGs)2 While involved in host antiviral defense, the products of ISGs are also potent regulators of cell growth and have increasingly complex immunomodulatory activities Numerous interferoninduced genes are involved in innate immunity3 The complex cross-signaling of cellular regulatory pathways involved in apoptosis, in ammation, and the stress response all are linked to the interferon pathway Cellular signaling pathways involved in the antiviral response have adapted due to the presence of viruses This observation illuminates a host repertoire for dealing with viral infection that is intriguingly complex There are two main types of interferon (IFN), type I and type II Type I IFNs include IFN-a, IFN-b, IFN-o, and IFN-t and are primarily produced in leukocytes These interferons are commonly called viral interferons and are a group of antiviral cytokines induced during viral infection by the viral replication processes.

A Textbook of Modern Toxicology, Third Edition, edited by Ernest Hodgson ISBN 0-471-26508-X Copyright 2004 John Wiley & Sons, Inc.

Fig. 15.7 Histogram (empirical density function) for interarrival time of one CMU and one external AT&T dataset.

A new recently described4 IFN-l and its class II cytokine receptor system may contribute to antiviral or other defenses by a mechanism similar to, but independent of, type I IFNs Type II IFN is IFN-g, which is produced only by certain cells involved in the immune response such as natural killer (NK), cytotoxic T cells (CD8 ), and CD4 T helper 1 (Th1) cells Not produced in direct response to the presence of virus, these IFNs are secreted when an infected cell is recognized as a part of the host s acquired immune response Type I and II IFNs share no obvious structural homology and have separate cell membrane receptors2 These receptors activate signal transduction pathways, which ultimately lead to the transcription of hundreds of interferon-stimulated genes (ISGs) There exists an overlap in the ISGs triggered by type I and type II IFNs.

Figure 11.1 Examples of exposure/effect scenarios that result in either acute toxicity (a), chronic toxicity (b), or mixed acute/chronic toxicity (c,d). Examples for each scenario are provided in the text.

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