Interaction of Influenza Virus with Blood Platelets

Abstract

The interaction of human blood platelets with influenza virus (PR-8) was studied in vitro and in vivo. It was found that "live" influenza virus was rapidly adsorbed onto human blood platelets at 4 C. and completely eluted at 37 C. "Dead" virus was adsorbed at 4 C. but not eluted at 37 C. unless the platelets were treated with RDE (receptor destroying enzyme). Adorption of virus also occurred at tem peratures above 4 C. (from 20 to 37 C.). However, while adsorption was maintained throughout incubation at 4 C., slow elution occurred after 30 to 90 minutes incubation at 26 to 37 C. Storage of the platelets for lengthy intervals at 4 C. or coating of the platelets with macromolecules did not interfere with virus adsorption. After one cycle of adsorption-elution, blood platelets could not adsorb virus again. Treatment with RDE greatly reduced virus adsorption. During the process of virus adsorption, prominent platelet clumping occurred. During elution, clumping remained unchanged, and gross alterations in morphology of the platelets were observed. In the process of virus adsorption-elution, large numbers of platelets were lysed. Comparative experiments were performed simultaneously with human red blood cells (RBC) and identical results were obtained as with blood platelets. However, the extent of adsorption of live virus was equal for platelets and RBC only when the relationship between platelet number and RBC number in the preparations used was 6:1. This suggested a direct proportion between the surface area of both platelet and RBC and the number of available virus receptors. Virus suspensions infused into rabbits produced a sharp and sustained drop of the platelet count. Survival of radioactively labeled platelets treated with virus prior to infusion was markedly shortened with live virus and was only slightly reduced with dead virus. It is suggested from these experiments that blood platelets, as other blood cells, may serve as carriers of viruses in the circulation and that in this process the platelets are damaged and partially destroyed.

Human platelets efficiently kill IgG-opsonizedE. coli

“…Previous reports from our group and others suggest that platelets can bind and internalize various targets of similar size to bacteria (Jerushalmy et al, 1961;Movat et al, 1965;Terada et al, 1966;Youssefian et al, 2002;Fitzgerald et al, 2006b;Antczak et al, 2011). In order to determine whether platelets bind E. coli, we incubated freshly washed human platelets with bacteria and assessed the viability using the Live-Dead BacLight kit and epifluorescence illumination.…”

Influenza viremia and the potential for blood‐borne transmission

“…Influenza has been shown to adsorb to PLTs and RBC with equal kinetics and to elute from PLTs more slowly and less completely than from RBCs 55 . Binding of live or dead influenza virus to PLTs in vitro caused morphologic signs of damage to the PLTs including swelling, ballooning, and fragmentation, with a pronounced decrease in PLT counts 56 . Intravenous infusion of influenza virus in rabbits caused transient thrombocytopenia to levels 50 percent of normal for 1 to 2 days' duration.…”

Characterization of platelet‐reactive antibodies in children with varicella‐associated acute immune thrombocytopenic purpura (ITP)

“…Transient thrombocytopenia fo llowing immunization with live-virus vaccines has also been described (Asano et al 1985). Thrombocytopenia may occur during the viraemic phase of viral infection (Morse et al, 1966;Terada et al 1966: Oski & Naiman, 1966 or. more commonly.…”

“…1990). rubella (Morse et al, 1966;Hudson et al, 19 54), Epstein-Barr virus (Grossman & Wolff, 1959), influenza (Terada et al 1966), and human immunodeficiency type 1 virus (HIV) (Ellaurie et al 1988). Transient thrombocytopenia fo llowing immunization with live-virus vaccines has also been described (Asano et al 1985).…”