Viral Susceptibility and Embryonic Differentiation.

Development ◽  
1963 ◽  
Vol 11 (4) ◽  
pp. 757-764
Author(s):  
Juhani Rapola ◽  
Tapani Vainio ◽  
Lauri Saxén

The fact that viral susceptibility changes during embryogenesis has been pointed out by both experimental embryologists and clinical practitioners, not to mention virologists working with avian material. In attempts to find the fundamental factors which make embryonic tissue susceptible or resistant to a given virus, the metabolic and proliferative rate have been considered relevant (Williamson et al., 1953; Robertson et al., 1955; Töndury, 1956). Experience accumulated in studies of the replication of various viruses in tissue culture has taught us that a high metabolic rate and active proliferation may not always enhance viral replication (Ginsberg, 1958). However, there seems to be justification for the view that an injurious agent leads to more severe tissue damage when it exercises its effect upon actively proliferating tissues than when it does so at the ‘resting stage’.

2011 ◽  
Vol 2 (1) ◽  
pp. 42-46 ◽  
Author(s):  
Andrea Y. Frommel ◽  
Rommel Maneja ◽  
David Lowe ◽  
Arne M. Malzahn ◽  
Audrey J. Geffen ◽  
...  

Cytotherapy ◽  
2018 ◽  
Vol 20 (5) ◽  
pp. S115
Author(s):  
A. Chapel ◽  
A. Semont ◽  
C. Linard ◽  
N. Mathieu ◽  
C. Demarquay ◽  
...  

2003 ◽  
Vol 51 (6) ◽  
pp. 603 ◽  
Author(s):  
M. P. Ikonomopoulou ◽  
R. W. Rose

We investigated the metabolic rate, thermoneutral zone and thermal conductance of the eastern barred bandicoot in Tasmania. Five adult eastern barred bandicoots (two males, three non-reproductive females) were tested at temperatures of 3, 10, 15, 20, 25, 30, 35 and 40°C. The thermoneutral zone was calculated from oxygen consumption and body temperature, measured during the daytime: their normal resting phase. It was found that the thermoneutral zone lies between 25°C and 30°C, with a minimum metabolic rate of 0.51 mL g–1 h–1 and body temperature of 35.8°C. At cooler ambient temperatures (3–20°C) the body temperature decreased to approximately 34.0°C while the metabolic rate increased from 0.7 to 1.3 mL g–1�h–1. At high temperatures (35°C and 40°C) both body temperature (36.9–38.7°C) and metabolic rate (1.0–1.5 mL g–1 h–1) rose. Thermal conductance was low below an ambient temperature of 30°C but increased significantly at higher temperatures. The low thermal conductance (due, in part, to good insulation, a reduced body temperature at lower ambient temperatures, combined with a relatively high metabolic rate) suggests that this species is well adapted to cooler environments but it could not thermoregulate easily at temperatures above 30°C.


BDJ ◽  
2005 ◽  
Vol 199 (7) ◽  
pp. 443-443 ◽  
Author(s):  
B Westbury
Keyword(s):  

1994 ◽  
Vol 179 (1) ◽  
pp. 101-113 ◽  
Author(s):  
M D Miller ◽  
M T Warmerdam ◽  
I Gaston ◽  
W C Greene ◽  
M B Feinberg

Considerable controversy and uncertainty have surrounded the biological function of the Human Immunodeficiency Virus (HIV)-1 nef gene product. Initial studies suggested that this early, nonstructural viral protein functioned as a negative regulatory factor; thus, it was proposed to play a role in establishing or maintaining viral latency. In contrast, studies in Simian Immunodeficiency Virus (SIV)mac-infected rhesus monkeys have suggested that Nef is not a negative factor but rather plays a central role in promoting high-level viral replication and is required for viral pathogenesis in vivo. We sought to define a tissue culture system that would approximate the in vivo setting for virus infection in order to assess the role of HIV-1 Nef in viral replication. We show that infection of mitogen-activated peripheral blood mononuclear cells (PBMC) with Nef+ HIV results in enhanced replication as evidenced by earlier gag p24 expression when compared with infections performed with nef mutant viruses. Moreover, when unstimulated freshly isolated PBMC are infected with Nef+ and Nef- viruses and then subsequently activated with mitogen, the Nef-induced difference in viral replication kinetics is even more pronounced, with the Nef- viruses requiring much more time in culture for appreciable growth. A positive effect of Nef on viral replication was also observed in primary macrophages infected with a recombinant of YU-2, a patient-derived molecular clone with macrophage tropism. These positive effects of Nef on viral replication are dependent on the initial multiplicity of infection (MOI), in that infections of unstimulated PBMC at low MOI are most dependent upon intact nef for subsequent viral growth. We now provide evidence that the Nef+ HIV is more infectious than Nef- HIV from both a tissue culture infectious dose analysis, and a single-cell HIV infection assay. In the latter case, we demonstrate that infection with equivalent doses of HIV based on virion-associated gag p24 yields five- to sixfold more infected cells if Nef+ viral stocks were used. Furthermore, we find that the differential infectivity is not dependent on CD4 down-regulation as Nef+ virus produced from transfected COS cells lacking CD4 is also more infectious. However, normalization of PBMC infections to equivalent infectivity between that of the Nef+ and Nef- viruses continues to reveal delayed viral replication in the absence of Nef, suggesting that secondary viral spread in PBMC is also enhanced in Nef+ infections. We demonstrate this directly by showing a 13-15-fold increase in infectivity of PBMC-derived Nef+ HIC.(ABSTRACT TRUNCATED AT 400 WORDS)


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