Morphological changes in human neural cells following tick-borne encephalitis virus infection.
J Gen Virol. 2009 Mar 4;
Authors: Ruzek D, Vancová M, Tesaøová M, Ahantarig A, Kopecky J, Grubhoffer L
Tick borne encephalitis (TBE) is one of the leading and most dangerous human viral neuroinfections in Europe and northeastern Asia. The clinical manifestations include asymptomatic infections, fevers and debilitating encephalitis that might progress into chronic disease or fatal infections. To further understand TBE pathology in host nervous systems, three human neural cell lines, i.e. neuroblastoma, medulloblastoma and glioblastoma cells, were infected with TBE virus (TBEV). The susceptibility and virus-mediated cytopathic effect including ultrastructural and apoptotic changes of the cells were examined. All the neural cell lines tested were susceptible to TBEV infection. Interestingly, the neural cells produced about 100-10,000-fold higher virus titer than the conventional cell lines of extraneural origin, indicating the highly susceptible nature of the neural cells to TBEV infection. The infection of medulloblastoma and glioblastoma cells was associated with a number of major morphological changes, including proliferation of membranes of the rough endoplasmic reticulum and extensive rearrangement of cytoskeletal structures . The TBEV-infected cells exhibited either necrotic or apoptotic morphological features. We observed ultrastructural apoptotic signs (condensation, margination and fragmentation of chromatin) and other alteration, such as vacuolation of the cytoplasm, dilatation of the endoplasmic reticulum cisternae, and shrinkage of cells accompanied with high density of the cytoplasm. On the other hand, infected neuroblastoma cells did not exhibit proliferation of membranous structures. The virions were present in both endoplasmatic reticulum as well as in the cytoplasm. Cells were dying preferentially by necrotic mechanism rather than apoptosis. Neuropathological significance of these observations is discussed.
PMID: 19264624 [PubMed - as supplied by publisher]