For this, 12 weeks after the primary immunization, guinea pigs were infected with 50 100 bacilli by aerosol route and euthanized at 10 weeks post-infection (Exp-I).
In case of saline treated animals at 10 weeks post-infection (Exp-I), extensive areas of collagen deposition in and around the granulomas were observed (Fig. 4A).
At 10 weeks post-infection (Exp-I), both vaccinated and saline treated guinea pigs showed a comparable fold induction of these cytokines at mRNA level (Fig. 8A).
At 16 weeks post-infection (Exp-II), the saline treated animals exhibited extensive granulomatous infiltration with coalescing necrotic granulomas (75%) effacing the pulmonary parenchyma (Fig. 3B).
At 16 weeks post-infection (Exp-II), 50% of the saline treated animals succumbed to the disease (3/6); animals that survived showed characteristic signs of end stage TB with extensive pathological damage (Fig. 2B).
At 10 weeks post-infection (Exp-I), severe pathological damage was observed in case of saline treated animals characterized by extensive involvement and numerous large tubercles with scattered areas of necrosis in both lung and liver (Fig. 2A).
However, at 16 weeks post-infection (Exp-II), a significant up-regulation of both the inflammatory cytokines (IFN-γ and TNF-α) was observed in BCG immunized guinea pigs (Fig. 8B), when compared to the saline treated animals (p<0.001).
Only one data set for mock-infection will be shown here as no mock-infection was done for Exp 3 and the shown data set is identical with the mock-infection of the data from mock-infection shown in the context of infections with the RKI virus.
Therefore the probability that A escapes infection from that child is exp(–0.00062 x 60) = exp(–0.0372) = 0.9635.
Mock-infection was omitted for Exp 3 to reduce experimental efforts.
Four weeks after LV-Exp-Htt infection, endogenous MSK-1 expression was slightly down-regulated (Fig. 1B, left panel, asterisk).
