Of 56 patients with symptomatic VTE, the relationship between VTE and immune dysfunction was found in 53 (94.6%). Nevertheless, patients with immune dysfunction do not develop symptomatic VTE in a short time. The compromised or disorganized immune function may be the internal cause of susceptibility to acquired VTE, and infection acts as a triggering factor of acquired VTE. When the pathogens invade the subjects with immune dysfunction, the pathogens can not be completely removed by the immune system. Thus, patients with compromised or disorganized immune function are susceptible to acquired VTE. Cedar Virus: A Novel Henipavirus Isolated from Australian Bats The genus Henipavirus in the family Paramyxoviridae contains two viruses, Hendra virus (HeV) and Nipah virus (NiV) for which pteropid bats act as the main natural reservoir. Each virus also causes serious and commonly lethal infection of people as well as various species of domestic animals, however little is known about the associated mechanisms of pathogenesis. Here, we report the isolation and characterization of a new paramyxovirus from pteropid bats, Cedar virus (CedPV), which shares significant features with the known henipaviruses. The genome size (18,162 nt) and organization of CedPV is very similar to that of HeV and NiV; its nucleocapsid protein displays antigenic cross-reactivity with henipaviruses; and it uses the same receptor molecule (ephrin- B2) for entry during infection. Preliminary challenge studies with CedPV in ferrets and guinea pigs, both susceptible to infection and disease with known henipaviruses, confirmed virus replication and production of neutralizing antibodies although clinical disease was not observed. In this context, it is interesting to note that the major genetic difference between CedPV and HeV or NiV lies within the coding strategy of the P gene, which is known to play an important role in evading the host innate immune system. Unlike HeV, NiV, and almost all known paramyxoviruses, the CedPV P gene lacks both RNA editing and also the coding capacity for the highly conserved V protein. Preliminary study indicated that CedPV infection of human cells induces a more robust IFN-β response than HeV. Henipaviruses were first discovered in the 1990s following investigation of serious disease outbreaks in horses, pigs and humans in Australia and Malaysia [1, 2] and comprise the only known Biosafety Level 4 (BSL4) agents in the family Paramyxoviridae [3] . Depending upon the geographic locations of outbreaks, and the virus and animal species involved, case mortality is between 40% to 100% in both humans and animals [4, 5] , making them one of the most deadly group of viruses known to infect humans. The genus Henipavirus in the subfamily Paramyxovirinae currently contains two members, Hendra virus (HeV) and Nipah virus (NiV) [6] . Fruit bats in the genus Pteropus, commonly known as flying foxes, have been identified as the main natural reservoir of both viruses although serological evidence suggests that henipaviruses also circulate in non-pteropid bats [7, 8, 9, 10] .