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. Author manuscript; available in PMC: 2012 Mar 15.
Published in final edited form as: Virology. 2011 Jan 20;411(2):288–305. doi: 10.1016/j.virol.2010.12.014

Figure 4. Increased susceptibility of young mice to coxsackievirus infection and subsequent CNS pathology.

Figure 4

Neonatal SJL mice (day 1, 2, or 6 post-birth) were intra-cranially infected with 100 pfu CVB3. The brains of infected mice were harvested on day 11, 15 or 33 post-infection, respectively. De-paraffinized sections of the brains were stained with hematoxylin and eosin and inspected by microscopy for lesions and inflammatory cells. (A) One day-old mice suffered the greatest level of neuropathology following infection. Lesions were observed within the cortex and hippocampus (black arrows). (B) A higher magnification of (A) revealed the loss of pyramidal neurons in the hippocampus and the presence of inflammatory cells (black arrows). (C) In contrast, two day-old mice infected with an identical amount of CVB3 showed reduce signs of neuronal loss restricted to the CA3 and CA4 field of the hippocampus (black arrow). The presence of immune cell enriched perivascular cuffs were observed near the hippocampus (black arrow). (D) Six day-old mice infected with CVB3 showed little or no signs of CNS disease.