Transbilayer phospholipid asymmetry and its maintenance in the membrane of influenza virus

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Abstract
Two phospholipid exchange proteins and 2 phospholipases C were employed to determine the phospholipid composition of the outer surface of the membrane of influenza virus. These 4 protein probes defined the same accessible and inaccessible pool for each viral phospholipid. Phospholipids which are exchangeable or hydrolyzable are located on the outer surface, whereas the inaccessible pool is located at the inner surface of the viral bilayer. The 2 pools are unequal in size, with about 30% of the total phospholipid accessible to the 4 proteins and about 70% inaccessible. The membrane is highly asymmetric with regard to the amount of phospholipid on each side of the membrane. There is also a marked asymmetry of phospholipid composition. Phosphatidylcholine and phosphatidylinositol are enriched in the outer surface and sphingomyelin is enriched in the inner surface. Phosphatidylethanolamine and phosphatidylserine are present in similar proportions in each surface. This distribution is qualitatively different from that previously reported for the human erythrocyte. The close agreement between results obtained with exchange proteins and phospholipases C demonstrates that the hydrolytic action of these enzymes does not alter phospholipid asymmetry. The nonperturbing nature of the exchange proteins permitted the rate of transmembrane movement of phospholipids (flip-flop) in the intact virion to be studied. This process could not be detected after 2 days at 37.degree. C. The half-time for flip-flop is indeterminately in excess of 30 days for sphingomyelin and 10 days for phosphatidylcholine at 37.degree. C. These extremely long times provide a simple explanation for the maintenance of transbilayer asymmetry in influenza virions and, possibly, other membranes. Since the viral membrane is acquired by budding through the host cell plasma membrane, the transbilayer distribution of phospholipids observed in the virions presumably reflects a similar asymmetric distribution of phospholipids in the host cell surface membrane. Because animal cells in culture do not incorporate extracellular phospholipid, individual cells have the capacity to generate asymmetric membranes.

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