Targeting Retroviral and Lentiviral Vectors

Pseudotyping lentiviral vectors with the wild-type measles virus glycoproteins improves titer and selectivity

“…They can be pseudotyped with glycoproteins from other enveloped viruses, in some cases after the truncation of cytoplasmic tails that interfere with particle incorporation. 1,2 The glycoprotein G of vesicular stomatitis virus (VSV) has widely been used for pseudotyping. 3 Recently, we achieved pseudotyping of lentiviral vectors with the envelope proteins of a vaccine strain of measles virus (MV).…”

Visualization of targeted transduction by engineered lentiviral vectors

“…[8][9][10] Many efforts have been made to develop such targeting viral vector systems mostly by altering the viral envelope glycoprotein. [11][12][13][14][15][16] Although certain envelope glycoproteins are structurally plastic enough to allow insertion of a new molecular recognition unit (such as peptide, single chain antibody, growth factor and so on) for targeting, this manipulation can adversely affect the delicate coupling interactions of the binding and fusion domains of glycoproteins, resulting in enveloped vectors with decreased infectivity to the target cells. 8,15,[17][18][19] We have previously developed an efficient method to target lentivirus-mediated gene transduction to a desired cell type.…”

Replicating retroviral vectors mediating continuous production and secretion of therapeutic gene products from cancer cells

“…The infectivity of retroviruses displaying foreign polypeptides as N-terminal extension of their SU protein depends on both the structure and the biological function of the displayed polypeptide. 37 Dimeric or trimeric molecules, for example, are more efficient in blocking infectivity than monomers (scFv molecules are usually monomers but can form dimers). On the other hand, monomers with high affinity for certain cell surface receptors can also strongly impair infectivity, while small peptides usually do not.…”

“…31,33 Second, the tumor microenvironment itself is known to be inherently immunosuppressive, and thus it is possible that RCR vector spread would be confined to the tumor tissue, while extratumoral spread would be restricted by the immune system. Furthermore, the tumor selectivity of RCR vector spread can be further improved by targeting vectors at different levels such as at cell entry 25,37,41 or incorporation of cell-type-and tissue-specific transcriptional control elements. [42][43][44] The availability of appropriately targeted RCR vectors would facilitate the design of therapeutically effective protocols for gene therapy of cancer.…”