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In an unconventional mechanism of interferon antagonism, NSs targets the RNA polymerase II (RNAP II) complex103 106 Rift Valley fever virus (RVFV), a phlebovirus of the family Bunyaviridae, is a major public health threat in Egypt and sub-Saharan Africa Bouloy and coworkers107 could show that the ability of RVFV to inhibit IFN-a/b production correlated with viral virulence, thereby suggesting that the accessory protein NSs is an interferon antagonist The nonstructural protein 5A (NS5A) of hepatitis C virus (HCV) has been implicated in inhibition of antiviral activity of IFN through both an interaction.

Fig. 15.15 Results of a connection-by-connection simulation of a connection-admission strategy for a single unit capacity edge contrasted for different interarrival time models. (a) 5214 arrivals taken from a one hour time period from an AT&T dataset. (b) 34,152 arrivals from a CMU dataset.

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This means that the Weibull distribution is modeling long breaks in the arrival process as least as well as a nonstationary Poisson process taken over a reasonable period. In addition, the Weibull process is capable of modeling the short interarrival times much more accurately. Figure 15.16 reveals some interesting comparisons of a nonstationary Poisson process to the stationary Weibull process. Figure 15.16(a) shows the actual arrival times of the connections for the arrivals derived from the June dataset. Figure 15.16(b) shows the empirical cumulative distributions of the original interarrival time distribution, the tted Weibull distribution, the tted exponential distribution, and the empirical distribution of the nonstationary Poisson process with period 6 minutes for the June dataset. While Fig. 15.16 shows the result for a speci c nonstationary Poisson process, the results are almost identical for other nonstationary Poisson processes.

Endocrine Disruptors (EDs)

between NS5A and the double-stranded RNA-dependent protein kinase (PKR), as well as the 20 ,50 -oligoadenylate synthetase (OAS).108,109 Both Newcastle disease virus (NDV) and Nipah virus possess interferon evasion proteins. The Nipah virus proteins V, W, and C all act to sequester STAT1, but V and P proteins act by retaining STAT1 in the cytoplasm while the W protein sequesters STAT1 in the nucleus.110,111 Dengue virus nonstructural proteins NS2A, NS4B, and NS4A have been shown to downregulate IFN-b-stimulated genes. NS4B at least may block IFN signaling during dengue virus infection by interference with STAT1 signaling.19

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Endocrine disruptors are compounds (synthetic and naturally occurring) that can alter the normal hormonal balance and function in animals. The historical ED diethylstilbestrol (DES) is a classic example of an endocrine disrupter affecting female reproductive health. In utero exposure of females to DES is associated with the induction of vaginal carcinomas apparent after puberty. In experimental mice, estrogenic substances cause accelerated sexual maturation and irregular estrous cycles and prolonged estrous. In rats, xenoestrogens such as kepone and methoxychlor cause masculinization of the exposed female rats. These rats do not ovulate, lack stimulation of the LH surge, and exhibit male sexual behavior. In humans, estrogen mimicking compounds can alter natural hormonal cycles and have been associated with breast cancer induction. Certain environmental EDs may function as promoters or inducers of carcinogenesis. Polychlorinated biphenyls (PCBs) and a trichloroethane compound (DDT) are persistent in the environment. Serum DDE (a DDT metabolite) levels have been found to correlate with breast cancer incidence.

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As previously described for the male reproductive toxicity, the class of toxicants affecting germ cells can alter the structure of genetic material (chromosomal aberrations, alterations in meiosis, DNA synthesis, and replication). Mature oocytes have a DNA repair capacity different from that of mature sperm, but this capacity decreases at the period of meiotic maturation.

Poxviruses, of intense interest for bioterrorism potential or as emerging natural infections (monkeypox), have devised at least six separate mechanisms to evade the interferon system. 1. Poxvirus infections lead to secretion of proteins that bind to type I or II IFNs.18,21,43,112 116 The IFN-binding proteins of myxoma virus and vaccinia have a sequence similar to the extracellular domain of the IFN-g receptor and bind to IFN-g. A type I IFN inhibitor has been reported in the supernatants and on the surface of cells infected with vaccinia and other orthopoxviruses. Mutant vaccinia viruses with a deletion of the type I IFN binding gene were attenuated in mice. 2. Orthopoxviruses contain a gene for a double-stranded RNA binding protein (E3L gene of vaccinia virus) that can block activation of PKR. Vaccinia virus E3L deletion mutants exhibit host range restriction, apoptosis, enhanced RNA degradation, and interferon sensitivity.31 34 This same dsRNA binding protein, since it soaks up dsRNA, can also block 2-5A synthesis by the dsRNA-activated 2-5A synthetase enzyme family. 3. Orthopoxviruses also can express an eIF-2 homologue (the K3L gene of vaccinia virus), deletion of which may enhance the interferon sensitivity of vaccinia virus. K3L acts as an eIF-2 decoy, thereby inhibiting eIF-2 phosphorylation and activation of PKR.35 37 4. IL-18 induced IFN-g production in macrophages and was able to protect mice from the pathological effects of vaccinia virus infection. An IL-18 binding protein (IL-18BP) is a soluble, secreted inhibitor of IL-18 produced by humans and mice presumably for regulatory purposes. Orthopoxviruses encode IL-18BP homologues that bind IL-18 and block IFN-g production.117 5. Vaccinia virus invokes several mechanisms to negate the effects of the RNase L activator, 2-5A (discussed above). 6. Poxvirus protein N1L inhibited NF-kB and interferon regulatory factor-3 (IRF-3) signaling.118

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