The SARS-CoV-2 pandemic has many parallels to the early days of the HIV epidemic. Both began with efforts to identify the causative pathogen, followed by rapid development of diagnostics, animal models, therapeutics, and preventive vaccines. After targeting of the gp120 and gp160 HIV envelope proteins proved ineffective, development of candidate vaccines to prevent HIV expanded to encompass DNA and viral vector vaccines, with the intent of inducing both humoral and cellular immunity. In recent years, mRNA has been harnessed as a newer platform for the development of candidate HIV vaccines.1 Advancing the evidence from HIV vaccines, research supporting vaccines against other pathogens has also influenced SARS-CoV-2 vaccine design, including structure-based design of stabilised epitope-scaffold proteins for respiratory syncytial virus,2 DNA vaccines for MERS-CoV,3 and ongoing global molecular surveillance for the design of influenza vaccines.4 Collectively, the knowledge gained through these preclinical, manufacturing, and clinical development experiences has allowed for a rapid pivot to apply these approaches to SARS-CoV-2 vaccine research. The success of several large efficacy trials of HIV candidate vaccines has been used to advance SARS-CoV-2 vaccine research and development via existing public–private partnerships and networks such as the HIV Vaccine Trials Network and their established connections with local investigators and community advocates.
The most noteworthy difference between responses to SARS-CoV-2 and HIV is the time to authorisation and rollout of effective preventive vaccines. Emergency use authorisation of initial vaccines against COVID-19 was granted by the US Food and Drug Administration and European Medicines Agency less than 1 year after initial publication of the genetic sequence of SARS-CoV-2. By stark contrast, after more than 30 years of research, only six efficacy trials of candidate HIV vaccines have been completed,5 of which only one showed partial efficacy in preventing acquisition of new HIV-1 infection (risk lowered by 31%).6 Much of this discrepancy is due to inherent biological differences between HIV and coronaviruses, such as HIV's substantially higher mutation rate due to reverse transcription and evasion of immune responses after HIV integration into the host genome. Nonetheless, there is much that can be learned from SARS-CoV-2 vaccine development to accelerate the current pace of HIV vaccine development.