Showing papers on "Dengue virus published in 1978"

Replication of dengue and junin viruses in cultured rabbit and human endothelial cells.

Abstract: The flavivirus dengue and the arenavirus Junin are both associated with a hemorrhagic shock syndrome in man. We have demonstrated the replication of these viruses in vitro in both rabbit and human endothelial cells by viral titers and immunofluorescent antibody studies. Rabbit endothelium established in continuous culture was derived from vena cava, while human cells in primary culture were derived from umbilical veins. In rabbit endothelium, dengue-2 virus passaged through monkey kidney monolayer cells (LLC-MK2) or human lymphoblastoid cells (raji) produced significantly more virus than the seed obtained from suckling mouse brain (MB). Inoculation of actively dividing, subconfluent human endothelial cells with the LLC-MK2 degue virus produced higher viral titers than inoculation of confluent cells. The appearance of Junin virus was delayed beyond that of dengue virus in rabbit endothelial cells although equivalent titers of virus were produced. In human cells, Junin virus was less productive than dengue virus and produced characteristic cycles of virus release. This is the first direct evidence for replication of human hemorrhagic fever viruses in endothelial cells.

Host defence mechanisms against dengue virus infection of mice.

Abstract: Summary Serum obtained from mice 3 to 5 weeks after the third i.p. dose of dengue type 2 virus (DV) protected recipient mice against intracerebral challenge with DV, whereas the serum obtained after 1 and 2 weeks provided minimum protection. Adoptive intravenous transfer of immune spleen cells obtained from mice 1 to 5 weeks after immunization did not protect recipient mice against even a small dose (10 LD50) of DV. Depletion of T-cells by treatment of mice with anti-thymocyte serum did not potentiate DV infection. Development of a cell-mediated immune response (CMI) against DV was noted only at two periods by the leucocyte migration inhibition test (LMI), with borderline values of 20 and 21%. Dengue virus did not cause illness or death in mice when given by i.p. or i.v. routes and this was not affected by pre-treatment of mice with silica to damage local macrophages. It is concluded that humoral antibody plays a critical role in recovery from primary dengue virus infection of mice whereas CMI and macrophages appear to have no protective role.

Ultrastructural studies on dengue virus infection of human lymphoblasts.

Abstract: Ultrastructural studies of dengue-2 virus-infected lymphoblastoid Raji cells showed that the virus induced an increase in the size of the rough endoplasmic reticula (RER) and that the replication of the virus was confined to the cisternae of these RER. The proliferating RER formed cytoplasmic inclusions that could be seen by light microscopy. This observation could be used as evidence of a cytopathogenic effect of dengue virus on infected Rajii cells in routine cultures. Accumulation of virions in the infected cells was minimal in comparison with other cell systems, however. Sporadic clusters of mature virions were often seen on the plasma membrane. These extracellular virions were distributed adjacent to the virus-bearing RER and were presumably released virions. Vertical transmission of the virus was evident in mitotic lymphoblasts. The replication pattern of dengue virus in lymphoblastoid cells suggests that efforts should be made to determine whether blast-transformed lymphocytes, numerous in secondary dengue infections, support dengue virus replication in vivo.

Dengue with haemorrhage and shock in Jakarta, Indonesia.

Abstract: Pediatric patients with fever and haemorrhage were studied in Jakarta, Indonesia between May 1973 and January 1974. Eighty-one of 104 demonstrated unequivocable evidence of dengue with clinical findings similar to those reported associated with dengue haemorrhagic fever in Thailand. The majority of patients had extremely high antibody titers against dengue measured by both hemagglutination-inhibition and by plaque reduction neutralization tests and all four types of dengue virus were isolated. Eight of the patients died.

A rapid fluorescent focus-inhibition test for determining dengue neutralizing antibody and for identifying prototype dengue viruses

Abstract: Neutralizing antibody to dengue virus in human and animal sera was assayed by the rapid fluorescent focus-inhibition test (RFFIT). Neutralizing-antibody titers could be detected after only 24 h com...

Dengue viral antigens in host cell membranes.

Abstract: Membranes from type 2 dengue virus (DEN-2) infected BHK cells, when used as immunogen, elicit antibodies detectable by complement fixation, hemagglutination inhibition and plaque reduction neutralization tests with suckling-mouse-brain-derived DEN-antigens. Membrane fractions from infected cells separated by sucrose density gradient centrifugation were employed as antigen in serological tests with anti-DEN-2 infected suckling mouse brain hyperimmune mouse serum and hyperimmune mouse ascitic fluid. Antigen (s) capable of fixing complement were associated with all membrane fractions, including the plasma membrane, whereas antigen capable of reacting with antihemagglutinin was largely confined to the two membrane bands consisting of (1) a mixture of rough and smooth endoplasmic reticulum (2) predominantly rough endoplasmic reticulum.

A dengue epidemic at Futuna

Abstract: During an outbreak occuring in Futuna (Horne Islands) from October 1976 to January 1977, II strains quite similar to dengue virus type I were isolated from blood of patients in acute phase. Immunitary responses were noted on 8/12 paired sera submitted to IH test; 4/17 serum samples showed antibody titer presumptive of a recent infection. Entomological survey gave evidence that virus was transmitted by Aedes polynesiensis and confirmed that Futuna is free of A.E. aegypti; other species found were: Culex annulirostris, C. pipiens fatigans, C. sitiens. A viral strain was isolated from Ae. polynesiensis only.

Effects of Ca++ ion on the liberation of dengue virus from BHK-21 cells in culture.

Abstract: The mechanism by which virus is liberated from infected cells is important for studying the process of virus infection. At least three possible ways of virus liberation are (i) reverse phagocytosis (exocytosis), (ii) disruption of cells (bursting) and (iii) budding from the cellular membrane. As for dengue viruses, there have been a few reports suggesting the exocytotic discharge of virus based on electron microscopic observations (1, 2, 5). It has already been reported that a high Mg++ concentration in a media of dengue-infected Vero cells enhances virus liberation from the cells (7). The mechanism underlying this phenomenon may probably be stimulation of the liberation of mature virus from the intracytoplasm to the extracytoplasmic space under the influence of the high Mg++ concentration in media (8). These facts prompted us to study the Ca++ dependency of dengue virus liberation from infected cells, which suggested that this phenomenon was due to an exocytotic process. A concept has been presented that exocytosis is the mechanism for the release of secretory substances from neuron, neurosecretory, endocrine, and mast cells and that Ca++ ion is essential for the release of secretions by this exocytotic process (10). If the virus liberation from cells is due to exocytosis, it might be possible that Ca++ ion dependency exists. We examined this possibility in the present work. Type 1 dengue virus (Mochizuki strain) (DEN) and, as a control, chikungunya virus (African strain) (CHIK) were used. It has been known that chikungunya virus is liberated from the cell surface membrane by the process of budding instead of exocytosis (4,6). We studied whether or not maintenance of cells in a Ca-free culture medium containing EDTA, a chelating agent, affected DEN liberation.

An epidemic of dengue fever in Wewak.

Abstract: 143 clinical cases of dengue fever were reported in Wewak between April and August 1976. 15 patients demonstrated a diagnostic rise in antibody titre for Group B arbovirus. Tests for complement-fixing antibody to dengue viruses did not indicate what type of dengue virus was responsible for the epidemic. Vector species Aedes aegypti and Aedes scutellaris were found before control measures were adopted but were not found four months later. The epidemiology of dengue fever is discussed and measures for prevention and control of epidemics are recommended.