"The viral network we have detailed is a snapshot
of the early stages of an epidemic,
before the evolutionary paths of
COVID-19 become obscured by vast numbers of mutations.
It's like catching
an incipient supernova in the act." - Peter Forster
The simian foamy
virus (SFV), a spumavirus, has been co-speciated with Old World primates for
about 30 million years, making them the oldest known vertebrate RNA (ribonucleic acid) or retroviruses.
late 1950's SV40, a retrovirus, is identified in
the injected form of the polio vaccine.
This is believed to be due to kidney
cells from infected monkeys being used to amplify the vaccine virus during production.
Both the Sabin vaccine (oral, live virus) and the
Salk vaccine (injectable, killed virus)
are affected; the technique
used to inactivate the polio virus in the Salk vaccine, by means of
formaldehyde, did not reliably kill SV40.
When two or more vaccines are
mixed together in the same formulation, the two vaccines can interfere.
This most frequently occurs with live attenuated vaccines, where one of
the vaccine components is more robust than the others and suppresses the growth
and immune response to the other
This phenomenon was first noted in the trivalent Sabin
polio vaccine, where the amount of serotype 2 virus in the vaccine had to be
reduced to stop it from interfering with the "take" of the serotype 1 and 2
viruses in the vaccine.
SIVagm is a lentivirus also a retrovirus.
The genome consists of two strands, a longer negative-sense strand and
a shorter and positive-sense strand of variable length.
In the virion
these strands are arranged such that the two ends of the long strand meet but
are not covalently bonded
The virus binds to receptors allowing viral particles to enter
This is then translocated to the nucleus, where the
partially double stranded DNA is 'repaired' by the viral polymerase to form a
complete circular dsDNA genome (called covalently-closed-circular DNA or
The genome then undergoes transcription by the host cell RNA
polymerase and the pregenomicRNA (pgRNA) is sent out of the nucleus.
The pgRNA is inserted into an assembled viral capsid containing the
Inside this capsid the genome is converted from RNA
to pdsDNA through activity of the polymerase as an RNA-dependent-DNA-polymerase
and subsequently as an RNAse to eliminate the pgRNA transcript.
new virions either leave the cell to infect others or are immediately
dismantled so the new viral genomes can enter the nucleus and magnify the
The virions that leave the cell egress through
This is a deoxyribonucleic acid virus.
1960s Researchers "isolate" and then inoculate with the MS-2 strain of
hepatitis B virus.
Hepatitis viruses replicates through an RNA
intermediate form by reverse transcription, and in this respect they are
similar to retroviruses.
Hepatitis B virus belongs to the Hepadnavirus
Hepadnaviruses have very small genomes of partially
double-stranded, partially single stranded circular DNA.
early 1970s African rhesus monkeys are used in the manufacture
of the hepatitis B vaccine.
Human hepatitis B viruses cultured
in vivo in rhesus monkeys are
returned to humans whose infected blood serum is then pooled to develop four
different strains of experimental hepatitis B vaccine.
experimental vaccine is pilot tested in New York City and central
Hepatitis B vaccine
recipients worldwide, including gay men in
New York, and Black Africans in Central Africa, are exposed to simian
viruses including SV40, SIVagm, and perhaps others.
neglected evolutionary route of SIVagm to HIV-1 zoonosis sequentially
a) human incubation for more than a decade of polio vaccine
contaminants and recombinants including SV40, SFR, and possibly
b) the pooling of infected blood serum donated by hundreds of
gay American and Black African
hepatitis B vaccine
recipients who had subsequently received injections with
cultured strains of hepatitis B
c) the biohazardous laboratory conditions and viral
containment problems reported by the hepatitis B vaccine investigators and their
This series of events provides the best explanation for an
early to mid-1970s "punctuated origin event" most precisely fitting
the etiological determinations
of the HIV-1/AIDS pandemic.
There is evidence demonstrating that the
associated retrovirus (SZRV) is an autoimmune disorder causing
retrovirus in the Type-D family of retroviruses, e.g., SRV-1 (simian retrovirus
type 1), SRV-2 (simian retrovirus type 2), M7 (baboon endogenous retrovirus),
SMRV-H (squirrel monkey retrovirus), HTLV (human T lymphocyte leukemia virus)
and distantly-related to HIV (human
A French team at the Pasteur Institute in Paris, France, led by Luc
Montagnier, publish a paper in Science describing a retrovirus they call
LAV (lymphadenopathy associated virus), isolated from
a patient at risk for AIDS.
|HIV vaccine development
presents unprecedented challenges on multiple levels, a reality, often
overlooked, that cannot be overstated. The chief challenge is that HIV is a
human retrovirus that replicates by irreversibly inserting its genes into the
host genome. Thus, HIV infection is established permanently in a matter of days
or perhaps even hours, and it cannot be cleared by primary or anamnestic
responses that occur after exposure. In addition to integrating into the host
genome, a second unique challenge is that HIV replicates in CD4+ T cells that
are key players in protective immunity not only to HIV itself but also to many
other pathogens (cf. ref. 10). These central features distinguish the path to
an HIV vaccine from the traditional design principles that led to successful
vaccines against other infectious agents. The inability of these principles to
yield an HIV vaccine became abundantly clear in six large HIV vaccine trials,
where efficacy was not observed. Strikingly, vaccination increased the risk of
infection in two of these studies that selectively targeted T-cell immunity,
providing a stark contrast between the development of conventional and HIV
Against this backdrop, what will it take to develop the first
protective vaccine against a human retrovirus?
1984 Robert Gallo, a researcher at the National Cancer Institute where he
worked for 30 years mainly as head of the Laboratory of Tumor Cell
Biology, and collaborators publish a series of four papers in
Science demonstrating that a retrovirus they claim to have isolated is
the cause of AIDS, HTLV-III, related to the leukemia viruses of Gallo's earlier
Method of continuous production of retroviruses
1987 Out of court settlement
between the National Institutes of
Health (NIH)and Pasteur Institute in Paris.
1991 Following years of controversy surrounding the out of
court settlement between the National Institutes of Health and the
Pasteur Institute, Gallo admits the virus he claimed to have discovered
in 1984 is in reality a virus sent to him from France the year before, putting
an end to a six-year effort by Gallo and his employer, the National
Institutes of Health, to claim the AIDS virus as an independent
1995 Gallo with his colleagues Paolo
Lusso and Fiorenza Cocchi publish their discovery that chemokines, a class of
naturally occurring compounds, are potent and specific HIV inhibitors.
This discovery was heralded by Science magazine as one of the
top scientific breakthroughs of the year.
The role chemokines play in
controlling the progression of HIV infection influences thinking on how AIDS
works against the human
1996 Gallo, Robert R. Redfield
and William A. Blattner, found the Institute of Human
2007 Gallo and his team are awarded
a $15 million grant from the Gates Foundation for
research into a preventive vaccine for HIV/AIDS.
2011 Gallo and his team received $23.4 million from a
consortium of funding sources to support the next phase of research into the
Institute of Human Virology's (IHV) promising HIV/AIDS preventive vaccine
The IHV vaccine program grants included $16.8 million from
the Gates Foundation, $2.2
million from the U.S. Army's Military HIV Research Program (MHRP), and other
research funding from a variety of sources including the National Institutes
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