We measured the cellular uptake of 125 I-labeled full-length Tat (amino acids 1 to 86) (125 I-Tat 1-86) and 125 I-Tat 1-72 (first exon) in human fetal astrocytes, neuroblastoma cells, and human fetal neurons and demonstrated that the uptake of 125 I-Tat 1-72 without the second exon was much lower than that of 125 I-Tat 1-86 (P < 0.01). This suggests an important role for the C-terminal region of Tat for its cellular uptake. 125 I-Tat uptake could be inhibited by dextran sulfate and competitively inhibited by unlabeled Tat but not by overlapping 15-mer peptides, suggesting that Tat internalization is charge and conformationally dependent. Interestingly, one of 15-mer peptides, Tat 28-42 , greatly enhanced 125 I-Tat uptake. These findings are important for understanding the neuropathogenesis of human immunodeficiency virus type 1 infection and in the potential application of Tat for drug delivery to cells.

Lumpy skin disease (LSD) is a highly infectious emerging viral disease of cattle and buffaloes in India. The main source of transmission of the disease is arthropods (mosquitoes, biting flies, Culicoides midges and three blood sucking hard ticks) which act as mechanical vector. Major clinical signs include skin nodules all over the body, fever, lacrimal discharge, nasal discharge, anorexia, decreased milk yield, emaciation, depression and reluctance in movement. Since the first report of lumpy skin disease in India, it is spreading rapidly across the country causing a possible threat to the cattle and buffalo population in terms of productivity and mortality.