Expanding HIV's Host Range: A Response

Editor’s note: Last November 30, we published an Opinion piece by Alexander Kohn, professor of virology at Tel Aviv University. In the article, Kohn questioned the wisdom of inserting the CD4 gene from HIV into cell lines, especially HeLa cells. Such research could, Kohn suggested, expand the host range of HIV In this response, Howard M Temin, of the McArdle Laboratory for Cancer Research, tries to lay Kohn’s concern to rest. We invite further comment. Alexander Kohn and the headl

By | April 4, 1988

Editor’s note: Last November 30, we published an Opinion piece by Alexander Kohn, professor of virology at Tel Aviv University. In the article, Kohn questioned the wisdom of inserting the CD4 gene from HIV into cell lines, especially HeLa cells. Such research could, Kohn suggested, expand the host range of HIV In this response, Howard M Temin, of the McArdle Laboratory for Cancer Research, tries to lay Kohn’s concern to rest. We invite further comment.

Alexander Kohn and the headline writer have changed the meaning of a term in their suggestion that the proposed work with HeLa cells would result in an expansion of HIV’s host range (“The Dangers of Expanding HIV’s Host Range,” November 30, 1987, p. 11). The work objected to would allow HIV to replicate in some modified HeLa cells. However, there is no evidence or even suggestion that such growth would result in a changed virus. Thus, the virus would not have an expanded host range in the usual sense of this term. The virus could merely grow on some additional laboratory cells. Culturing more T4-positive human cells would also provide additional cells for HIV growth. Stated in this way, it is clear that there is no safety problem with this experiment.

Two interesting questions are raised in the article. The first relates to the statement that “HIV mutates at least five times more rapidly than the notoriously changeable influenza virus.” Again, we must be careful of our terms. What is referred to is the fact that numerous variants of HIV exist in the human population. However, we do not know whether this variability reflects a higher mutability of the virus (which is unlikely), high selection against specific viruses, or many cycles of virus replication. Thus, this observation points to a problem for vaccine development, not a future, more infectious pathogen.

However, this raises the second interesting question: What is the chance that HIV may become infectious by routes other than those already known? (Again I must reiterate that growing the virus in HeLa cells will not affect this possibility. HIV is growing in millions of people, so if such variants can appear, there is ample opportunity for them to do so.) HIV is currently such a serious problem because it infects CD4-positive infects CD4-positive cells and results in their death. A change in the virus so that it used another receptor or, for example, had a higher level in saliva resulting in a different mechanism of spread would result in a different cell tropism. Thus, such a variant virus would not cause AIDS.

Therefore, I do not think a variant HIV with new modes of spread is likely. However, this is not grounds for optimism. The HIVs we have are bad enough.

Temin is with the McArdle Laboratory for Cancer Research, University of Wisconsin Medical School, 450 N Randall Ave., Madison, WI 53706. In 1975 he shared the Nobel Prize with David Baltimore and Renato Dulbecco for their work on the interaction between tumor viruses and the genetic material of the cell.


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